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Year : 2018  |  Volume : 62  |  Issue : 12  |  Page : 1004-1005  

Atypical prolonged spinal anaesthesia

1 Department of Medicine, All India Institute of Medical Sciences, New Delhi, India, India
2 Department of Anesthesiology, Cleveland Clinic, Cleveland, Ohio, USA

Date of Web Publication10-Dec-2018

Correspondence Address:
Dr. Ursula Galway
Department of Anesthesiology, Cleveland Clinic, Cleveland, Ohio 44195
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ija.IJA_527_18

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How to cite this article:
Shergill S, Galway U. Atypical prolonged spinal anaesthesia. Indian J Anaesth 2018;62:1004-5

How to cite this URL:
Shergill S, Galway U. Atypical prolonged spinal anaesthesia. Indian J Anaesth [serial online] 2018 [cited 2021 Jan 24];62:1004-5. Available from: https://www.ijaweb.org/text.asp?2018/62/12/1004/247128


Spinal anaesthesia involves the injection of local anaesthetic into the subarachnoid space. We report an atypical case of a patient in whom spinal anaesthesia with 0.75% hyperbaric bupivacaine with fentanyl and epinephrine took over 17 h to regress.

The patient was a 21-year-old male weighing 102 kg and 185 cm tall with no known comorbidities, who was undergoing removal of left knee implant. The preoperative biochemical and laboratory parameters as well as vital signs were normal. The patient was placed in sitting position. Under sterile conditions, the L3–4 level subarachnoid space was accessed with a single puncture, using 25-G Whitacre spinal needle. The accurate placement was confirmed by the free flow of cerebrospinal fluid (CSF) before and after injecting 2 cm3 of hyperbaric 0.75% bupivacaine with 25 mcg of fentanyl and 200 mcg epinephrine. Initial post-placement vitals were stable. A T6 level of anaesthesia was achieved and surgery commenced. Propofol infusion was started at a rate of 10 μg/kg/min, increasing up to 50 μg/kg/min. After the incision, patient received a single dose of 10 mg ephedrine to counter a sudden fall in BP to 80/50mmHg. The patient maintained haemodynamic stability throughout the procedure which lasted about an hour.

Three hours postspinal placement, sensory anaesthesia level was at T12–L1 with no motor function of lower extremities. Six hours postspinal placement, the level regressed to L1 with minimal gross motor movement. Fentanyl was administered for mild back pain. His bladder was catheterised due to an inability to void. Nine hours postspinal placement, the sensory dermatomal level was at L1–L2. He could move his toes but struggled to lift legs off the bed. Twelve hours postspinal placement, he was able to raise legs on both sides. The sensory level had resolved to L2 bilaterally. Due to the fact that the spinal was regressing albeit slowly, imaging was deferred, and neurological checks were continued every 2 h. After 17 h postspinal placement, the patient had a return of normal sensation and motor strength throughout his lower limbs.

The effect of anaesthesia in this case lasted about four times the reported duration of recovery for bupivacaine doses ranging from 7.5 to 15 mg (150–240 min for pinprick sensation recovery at S2 and 84–120 min for motor block).[1] We used a 15-mg dose of hyperbaric bupivacaine (standard for our institution is 10–15 mg) along with epinephrine and fentanyl as adjuncts. Additives like fentanyl help reduce the dose of local anaesthetic due to synergistic analgesia for somatic and visceral pain from both the opioid and local anaesthetic.[2] Adding vasopressors like epinephrine helps prolong the motor and sensory anaesthesia duration which might extend recovery from the block.[3] Cases of prolonged spinal blocks should be promptly evaluated for anterior spinal artery (ASA) syndrome, cauda equina syndrome, spinal haematoma formation and transient radicular irritation (TRI) to prevent irreversible neurological injury.[4] Our patient had no pain or paraesthesia during spinal puncture, decreasing the likelihood of a nerve injury. Spinal haematoma was of low probability since spinal puncture was a single, atraumatic attempt with no history of anticoagulant medication. With complete sensory and motor sensation loss, both TRI and ASA syndrome were low probability since there is some sparing in both.[4] In our case, a low CSF volume is a suspected cause for prolonged block, as previously reported by Arndt and Downey where administration of 7.5 mg hyperbaric bupivacaine and 25 mcg fentanyl lead to a 36-h long block.[5] A study shows that CSF volume is inversely correlated to regression of the block as high amount of CSF leads to dilution of the anaesthetic injected in the space.[6] A possible higher concentration of the CSF could have been explained by testing the CSF or imaging study to see any bony abnormalities or presence of narrowed space like cyst. Unfortunately, no such studies were done in our patient, making the theory of a smaller CSF space just one hypothesis. Alternatively, the addition of a vasoconstrictor to increase the duration of action of a block (in our case the addition of epinephrine) had achieved its purpose of prolonging the block but for exceptionally longer than expected. In conclusion, an unexpectedly prolonged spinal block can be seen with regular doses of hyperbaric bupivacaine. Patient should be carefully monitored for development of neurologic symptoms needing urgent action to prevent permanent damage which can be catastrophic for the patient.

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There are no conflicts of interest.

   References Top

Liu SS, Ware PD, Allen HW, Neal JM, Pollock JE. Dose-response characteristics of spinal bupivacaine in volunteers. Clinical implications for ambulatory anesthesia. Anesthesiology 1996;85:729-36.  Back to cited text no. 1
Hamber EA, Viscomi CM. Intrathecal lipophilic opioids as adjuncts to surgical spinal anesthesia. Reg Anesth Pain Med 1999;24:255-63.  Back to cited text no. 2
Chiu AA, Liu S, Carpenter RL, Kasman GS, Pollock JE, Neal JM, et al. The effects of epinephrine on lidocaine spinal anesthesia: A cross-over study. Anesth Analg 1995;80:735-9.  Back to cited text no. 3
Horlocker TT. Complications of spinal and epidural anesthesia. Anesthesiol Clin North America 2000;18:461-85.  Back to cited text no. 4
Arndt JA, Downey T. Exceptionally prolonged anesthesia after a small dose of intrathecal bupivacaine. Anesthesiology 2002;97:1042.  Back to cited text no. 5
Higuchi H, Hirata J, Adachi Y, Kazama T. Influence of lumbosacral cerebrospinal fluid density, velocity, and volume on extent and duration of plain bupivacaine spinal anesthesia. Anesthesiology 2004;100:106-14.  Back to cited text no. 6


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