Blog with interesting cases and/or problems related to anesthesia with discussion based on best evidence in the literature.

November 14, 2018

34 year old female who is 15 weeks pregnant for cerclage

A 34 year old female required cerclage for incompetent cervix and presented to the OR for the procedure.  I discussed the pros and cons of GA vs. regional neuraxial anesthesia and we proceeded with spinal anesthesia.  The patient was taken to the OR, 6.5mg of hyperbaric bupivacaine + 20 mcg fentanyl was administered via 25 G whitakre needle.  The patient remained seated for aproximately 1 minute and then was layed supine. The patient tolerated the procedure without sedation.

The patient went to PACU able to move her legs but complaining of sinificant pruritis for which she requested treatment.  She was discharged after  2 hours and 37 min in the PACU after a case that was 30 min in duration.  

Management of the pregnant patient brings about a lot of questions for the anesthesiologist. Determining what anesthetics are safe and if needed what can be used to treat common side effects of anesthesia must be considered.  For example, in our patient, pruritis is typically treated with benadryl.  This medication may not be appropriate for the parturient however.  In general, I prefer to provide spinal anesthesia for cerclage. While there is currently no evidence to indicate that anesthetics are teratogenic, there is a growing literature demonstrating that anesthetics are neurotoxic to the fetus or early developing brain. While large human studies in pediatric patients seem to indicate that there is no significant increased risk to the brain, we have no good studies to indicate that there is not alteration to neurogenesis in the fetus.  Furthermore, even though we do not have evidence of harmful fetal affects of anesthetics, we also lack good solid randomized controlled trials to prove an absence of negative effects.  If you perform an anesthetic on a patient who is pregnant who goes on to deliver a newborn with obvious defects, not otherwise explained, you carry potential legal risk unless you can establish that general anesthesia was truly your only option.  

Giving spinal anesthesia to a patient who is to be discharged the same day creates panic in surgeons and facility administrators who are convinced that the patient will require prolonged care due to inability to void.  Therefore, in some cases overcoming this concern can be prohibitive.  Avoiding prolonged PACU stays (due to post operative urinary retention [POUR]) is accomplished by modification of typical intrathecal doses.

The control of micturition is a complex process involving multiple afferent and efferent neural pathways, reflexes and central and peripheral neurotransmitters.  It is well known that bupivacaine and tetracaine delay return of bladder function beyond the resolution of sensory anesthesia, and may lead to distention of the bladder beyond its normal functioning capacity.  This may result in bladder damage. The normal bladder has a capacity of between 400 mL and 600 mL.  The detrusor muscle is innervated by efferent somatic, sympathetic and parasympathetic fibers.  The parasympathetic fibers cause contraction of the detrusor and relaxation of the spinchter, permitting micturition. The sympathetic fibers produce detrusor relaxation and internal urethral sphincter closure.  The two systems are governed by spinal reflexes and two pontine brain stem centers. General anesthesia casues bladder atony. Volatile anesthetics as well as sedative-hypnotics inhibit  the pontine micturition center and voluntary cortical control center of the bladder.  IT injection of bupivacaine will block afferent and efferent neural transmission from and to the spinal segments (S2-S4).   Typically, complete normalization of detrusor strength occurs 1 to 3.5 h after ambulation. IT injection of opioid decreases the urge sensation and detrusor contraction largely by opioid effect on opioid receptors in the spinal cord that decrease parasympathetic firing.  Theses effects as well as others, can be reversed with naloxone administration. It is understood that opioids added to IT local anesthetic increases the rate of POUR.   This concept was looked at in an article by Niazi et al. [1].  They compared three groups of patients who received hyperbaric bupivacaine 0.5% (15 mg) (S1), bupi 15 mg + fentanyl 20 mcg (S2) or GA (G).  The incidence of POUR was 20% in group S1, 35% in group S2, and 8% in group G.  There incidence of 35% of POUR in the local + fentanyl group was much higher than another study [2] where the group with fentanyl given IT had POUR of only 20%.  This is likely because in this study only 7.5 mg of bupivacaine was used and 25 mcg of fentanyl.  The impact of bupivacaine dose was considered in a study that compared bupivacaine with lidocaine for spinal anesthesia for cervical cerclage.  In this study, the bupivacaine dose was 5.25 mg with 20 mcg of fentanyl added.  This was compared to lidocaine 30 mg + fentanyl 20 mcg [3]. They did not detect any difference between the two anesthetics with regard to onset and recovery time. They concluded that low dose bupivacaine (5.25 mg) offered a similar recovery profile to lidocaine IT 30 mg.  They did have 2 of 30 women in the lidocaine group with complaints consistent with TNS that resolved in 48 hours.  Indeed, lidocaine is really the gold standard in regards to outpatient spinal anesthesia.  Due to its reputation of causeing TNS, it has fallen into disuse.  TNS or transient neurological symptoms is described as transient buttock pain, radicular lower extremity pain, and dysesthesias that present within the first 24 hours following recovery from spinal anesthesia.  Some have reported an incidence as high as 40% with lidocaine. There is also some who speculate that the hyperbaric lidocaine solution (5% hyperbaric could be the cause) of TNS.  A recent study of  50 patients using 2% isobaric lidocaine as a single IT dose did not find a single case of TNS [4].  Unfortunately, this paper did not disclose the lidocaine dose.  This is important, because some studies suggest that the incidence of TNS is dose dependent [6].  In fact, some research or analysis of research suggests that using a lidocaine dose of less than 25 mg might prevent TNS from lidocaine.  The above study failed to cite another study performed in 1998 (Anesthesiology [5]). In this publication isobaric lidocaine 60 mg at a 2% concentration was compared to mepivacaine 1.5 %.  They found a 22.2% incidence of TNS with this formulation of lidocaine vs 0% in the mepivacaine group.  Another group used 10 mg lidocaine for spinal anesthesia and found a 0% incidence of TNS [7] with good operating conditions for prostate bx.  Another group compared knee arthroscopy in patients who received IT unilateral  bupivacaine 3 mg + fentnayl 10 mcg vs bilateral lidocaine 20 mg + fentanyl 25 mcg [8].  In this study no patients in either group suffered TNS (each group had n=25).  The incidence of pruritis was 5/25 patients and 7/25 patients in the bupi group vs the lido group.  Urinary retention not requiring bladder catheterization was found in 2/25 patients in the bupivacaine group (however the p value was 0.149).  They reported 100% excellent operating conditions for knee arthroscopy, with a duration of sensory block of 157 min in the bupivacaine group and 129 min in the lidocaine group. Time spent in the PACU was 39 min vs 0 min in the bupivacaine vs lidocaine group, time to ambulate was 159 min vs 3.6 min and time to home readiness was 184 min vs 153 min in the bupivacaine vs lidocaine group respectively.  while this was a small study, it seems to emphasize that with 20 mg of lidocaine + fentnayl, you can achieve a very short PACU stay, nominal risk for urinary retention, with very low chance of TNS.  Unfortunately, in many institutions, spinal lidocaine is simply not available.  Therefore, low dose bupivacaine is an alternative.  I opted for 6 mg of bupivacaine, but as mentioned there is some evidence that 5.25 mg of bupivacaine is sufficient for cerclage.  

1.  Niazi AAA, Taha MAA. Egyptian Journal of Anesthesia. 2015. 31:65-9.

2. Gupta A, Axelsson K, Thorns, E, et al. Acta Anaesthesiol Scand 2003;47:13-9.

3. Beilin Y, Zahn J, Abramovitz S, Bernstein HH, Hossain S, Bodian C.  Anesth Analg. 2003; 97: 56-61.

4. Frisch NB, Darrith B, Hansen DC, Wells A, Sanders S, Berger RA. Arthroplast Today. 2018;4:236-39.

5. Liguori GA, Zayas VM, Chisholm MF. Anesthesiology 1998. 88; 619-23.

6. Buckenmaier CC III, Nielsen KC, Pietrobon R, et al. Anesth Analg 2002;95:1253-7.

7. Nishikawa K. et al. Jour of Clinical Anesthesia 2007;19:25-9.

8. Hassan HIEA, Anesth Essays Res 2015. 9:21-27.

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