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ASK THE EXPERTS: OBGYN

Many of my obstetric mothers suffered from shivering following epidurals. What are some of the proven and consistent methods to prevent or reduce the shakes once they occur? —gmceltm@hotmail.com

Dr. Joy Steadman responds:

The mechanism of shivering after epidural placement may most likely be due to peripheral vasodilation. Blood cooled in the periphery makes its way back to the hypothalamus, which detecting the temperature change signals the shivering response. The hypothalamic reset may be the source of elevated temperature coincident with labor epidural analgesia. Numerous strategies have been employed, none with 100% success. Keeping the ambient temperature of the room closer to mother's basal temperature, placing warm towels around the patient's head, using a hot-air blanket, infusing warm intravenous fluids. I even had a resident give 12.5mg of Demerol to stop particularly violent shivering in a patient. Demerol epidurally has been used successfully,( 25mg of preservative-free Demerol) along with larger doses of epidural fentanyl (100mcgs or Sufentanil 50mcgs). Fortunately the shivering is more of a nuisance than a danger in most parturients. However, in a patient with cardiomyopathy or other disease process where excess oxygen utilization could be very deleterious, it might be prudent to treat.


In my obstetric anesthesia residency, I notice that in the delivery room there is always a set of drugs ready in syringes: thiopental, atropine, sux, ephedrine. Why do we have to change the drugs daily? How much degradation of the drugs is expected? —kwti@rogers.com

Dr. Joy Steadman responds:

This is less a question of degradation than it is policy and protocol. Established policy is not always based on exact science or evidence-based medicine. However, getting people to refill syringes every day or so also has a way of making them check to see IF medications are in fact ready. In an area like OB or Trauma, having medications drawn and ready helps decrease medication errors in stat situations as well as decreasing the extra time it takes to draw up meds.

Pressor agents that come in brown vials may be light sensitive and thus lose potency within 24-48 hours. West Virginia University showed that Thiopental left out for 8 days doesn't support bacterial growth. Succinylcholine begins to lose potency when left unrefrigerated more than 28 days.


In my hospital there is currently a discussion about CNS pathologies and labour analgesia. Recently, I successfully performed this procedure in a patient with an history of multiple sclerosis, following the recommendation of R. Miller's "Anesthesiology" textbook in which the author says that there are only medico-legal implications related to the possibility of a new reactivation of the pathology in the period after the delivery. My question is: It is possible to have real guidelines about this feature? I didn't find it and the literature seems to indicate that this topic remains controversial. —Marco Traversa

Guest Editor Dr. Joy Steadman, Director Obstetric Anesthesia, University of Miami responds:

No single group has convened to set guidelines for the treatment of pregnant patients with regional analgesia or anesthesia. SOAP would be the logical choice. (ASRA gave us guidelines for doing regional anesthesia in the face of various anticoagulants/antiplatelet drugs with some controlled studies and many case reports/case series.)

2) Let's analyze what we know about local anesthetics in general. Toxicity is dose and time-exposure related. Therefore use the smallest dose or concentration that is efficacious for the least amount of time possible. Lidocaine causes more cellular apoptosis (cell death) than bupivicaine, the most likely explanation for the more frequent presence of Transient Neurologic Symptoms (TNS) after lidocaine than after bupivicaine. Finally, there may not really be that much difference in where local anesthetics work (or do their damage) and TNS has occurred after epidurals.

1. What do we know about exacerbations of MS?

  • 3-6 months postpartum regardless of anesthesia/analgesia is the time for relapse and has to do with hormonal milieu, stress/lack of sleep associated with a new baby, loss of immunomodulation of pregnancy.
  • An increase in core temperature by as little as one degree can cause a relapse of MS. Labor epidurals ARE associated with an increase in body temperature, regional anesthesia in the OR is associated with a decrease in body temperature. Therefore, monitoring temperature and preventing its rise would seem to be important.
  • Exacerbations can be treated with methylprednisolone, plasmapheresis, and possibly IFN-Beta therapy.
2. Opioids in clinically relevant doses do not cause any histologic changes AND they decrease the dose of local anesthetic required for pain control.

3. Other disease states with demyelination as a feature include Guillian-Barre and HIV, and pain syndromes with these diseases are successfully treated with local anesthetics without further extension of disease. So if we were to set up a set of guidelines for analgesia or anesthesia for MS I suggest the following:
  1. The patient must understand the likelihood of a relapse post-partum 3-6 months is part of the natural history of the disease.
  2. Plans should be made in advance that this patient has social support to help in the post partum period so that she does not get fatigued or stressed.
  3. Plans to treat her exacerbation should be ready in advance so that there is no delay in starting treatment.
  4. Bupivicaine/levobupivicaine should probably be favored over lidocaine.
  5. Patients should be kept normothermic (or even a little cool) to prevent exacerbation secondary to rise in core temperature.
  6. Elective section provides a brief exposure to local anesthetic. Narcotic CSE for labor with later activation of a very dilute solution of local anesthetic with narcotic would be reasonable for labor analgesia. I would attempt to minimize length of exposure time, which means the Obstetrician needs to be educated about our end of concerns so as to manage the labor in accord.
  7. Nursing needs to understand our concerns as well so that they don't warm the patient or insist on a
  8. I would probably forego lidocaine as my test dose and use levobupivicaine 0.5% instead.



I am an OB/GYN, and I recently admitted a 32 y/o G1P0 with gestational diabetes at 40 wk for elective cesarian. She had no history of surgeries, hx, penicillin allergy or esophageal reflux. For surgery, spinal anesthesia was applied as the first intervention without complication. During surgery she presented with a mild tachycardia of 140-160 that was reslved with ephedrine. Surgery lasted 28 min. without complication. Immediately after surgery, the patient complained of headache and one minute later develop sudden bilateral blindnes, with no other neurological deficit found after thorough evaluation. Approximately half an hour later she developed a tonic clonic seisure, tx valium 5mg iv. She had normal BP, no proteinuria, normal liver enzymes and coagulation profile, so pre-eclampsia/eclampsia was excluded as an etiology. Head CT done with normal results. She remained stable, and the blindness continued for about 12h then resolved completely, with no further symptoms or seizures. Could this transient blindness be a reaction due to the spinal anesthesia? —gmvelasco@hotmail.com

Dr. Peter Dwane responds:

This blindness is almost certainly not related to the spinal anesthetic. I agree that you have ruled out preeclampsia/eclampsia. Also, the fact that the blindness was transient, there were no other localizing neurological signs, and the CAT scan was normal, I believe, points to a reversible vascular incident. Examples of this could be a cortical migraine headache (CM), or hypertensive encephalopathy (HE).

If the patient's blood pressure (BP) was normal to elevated when you gave the ephedrine it would have increased the BP transiently, potentially causing HE. If you know that the BP was low before giving the ephedrine and/or did not increase above 150/90, HE would be unlikely and CM would be more likely.

"Migrainous phenomena can involve the occipital lobes and manifest with transient hemianopic phenomena, with or without scintillations or phosphenes, followed by headache. Hypertensive encephalopathy ... can produce cortical blindness or transient hemianopias in patients of any age."

Reference:

  1. Chapter 8 - Cranial Nerve II and Afferent Visual Pathways, P118. Goetz: Textbook of Clinical Neurology, 1st ed., Copyright © 1999 W. B. Saunders Company


What is the protocol for the epidural analgesia for labour pain if I want to use 0.0625% of bupivicaine+ fentanyl 2mcg/ml. Is it adequate if I do like this, test dose with 4 mls of 0.25%\ Bupivacaine, if nothing happens I give a bolus of 5 ml of 0.25% Bupivacaine and to start infusion with Bupi 0.0625%+Fentanyl 2 mcg/ml at 10 – 15 ml/hour? The peroneal pain in 2nd stage is treated with 5 ml of 0.25% Bupi. —basrimatnor@hotmail.com

Dr. Peter Dwane responds:

The protocol which you suggest is adequate and safe, but I believe that will negate the effect you are trying to achieve—less motor block—inusing the test dose and initial bolus of 0.25% bupivacaine. If you plan to use the infusion of Bupi 0.0625%+Fentanyl 2 mcg/ml at 10 – 15 ml/hour, I would suggest that your test dose could be 7.5 cc of this solution, followed in two minutes by a second bolus of 7.5 cc s, if there is no sign of subarachnoid injection– for a total initial injection of15cc. Then start your infusion. You may even want to increase the total volume of the initial test dose and boluses to 20 cc , or add another 20 – 25mcg of fentanyl to this 15 – 20 cc volume, if you wish to increase the success rate of your epidurals.Again, for the delivery, you may want to try using 0.125% bupivacaine 7.5cc + 50 mcg fentanyl as your peroneal dose, if you have sacral spread ofyour epidural infusion before the delivery. If your epidural hasn't reachedthe lower sacral roots as the presenting part descends then your dose of0.25% bupivacaine would be good, but again you might want to add the 50 mcgof fentanyl to increase the analgesic effect.


A 36 weeks pregnant patient with intense jaundice and INR of 1:1.9 is due for C-section. How should we proceed? What complication can we expect & how can we deal with them? —rajsound@yahoo.com

Dr. Peter Dwane responds:

Initially you should work with the patient's obstetrician and internist (gastroenterologist) to decide the cause of the patients disease. Through conventional history, physical and laboratory data, decide whether this is a medical and/or obstetric problem. The underlying cause of her jaundice is most likely hepatocellular or obstructive, and may also be related to the pregnancy: HELLP syndrome of severe preeclampsia, or acute fatty liverof pregnancy.

While you define the nature of the pathology and its severity you can begin supportive care for mother, and the obstetrician/pediatrician will follow up on prevention of vertical transmission of agent to the fetus is the cause is viral.

The medical team will be correcting the results of the hepatic derangements if severe: encephalopathy; coagulopathy; hypoglycemia; fluidand electrolyte abnormalities; decreased renal function and anemia. The patient should be delivered expeditiously, if this jaundice has been caused by the pregnancy.

Anesthetic problems (in addition to the above mentioned medical issues), if the hepatic disease is severe, could include: altered drug distribution and metabolism/excretion; hypoxemia due to intrapulmonary shunting, hypotension from peripheral shunting. If coagulopathy or esophageal varicesare present at the time of surgery, massive hemorrhage may also occur. General anesthesia should be used for a surgical procedure if there is ongoing encephalopathy or coagulopathy.


Should a pregnant patient with Arnold-Chiari Malformation Type 1 be allowed to undergo labor and delivery with an epidural, or is it best to schedule an elective C-section under general anesthesia? —kasarda@aol.com

Dr. Peter Dwane responds:

Arnold-Chiari malformation Type 1 is characterized by the partial descent of the medulla and cerebellar tonsils through the foramen magnum. This malformation carries with it a risk of increased intracranial pressure(ICP), which may be asymptomatic. Cough-induced headache may also bepresent.

This patient should be assessed by a neurologist or neurosurgeon because this uncommon condition needs to be specifically evaluated. Then there should be discussion among this neuro-specialist, the Obstetrician, and Anesthesiologist. Discussion would likely center around avoiding situationswhich might increase the pressure above the lesion relative to below the lesion… i.e. increasing the ICP with CNS depressants after a general anesthetic, or lowering the spinal pressure with a dural puncture. For the same reason the patient may be better of not bearing down during delivery. There are no series reporting the superiority of one anesthetic technique over another. My initial inclination would be toward general anesthesia for Cesarean section. But the specifics are best worked out by the three specialists involved.

References:

  1. Nel MR Robson V Robinson PN. Extradural anaesthesia for caesarean section in a patient with syringomyelia and Chiari type I anomaly. British Journal of Anaesthesia. 80(4):512-5, 1998 Apr.
  2. Semple DA. McClure JH. Arnold-chiari malformation in pregnancy. Anaesthesia. 51(6):580-2, 1996 Jun.


Is it dangerous to use electrocautery in Cesarean section (can it cause fetal seizures, amniotic aspiration, etc.) through auditory stimuli. —titodoc@yahoo.com

Dr. Peter Dwane responds:

In my anesthesia practice for the last 30 years I have not encountered concern for electrocautery during C/Section, with regards to it being acause of fetal seizures. Searching Medline, I could not find any reference to an association between fetal seizures and electrocautery Also, during neurosurgery, cautery is used directly on cerebral tissue without causing seizures in our anesthetized patients.


What is the current thinking on the subject of regional anesthesia for c-section or labor analgesia in the patient with genital herpes? —jfox@cmmc-snc.com

Dr. Peter Dwane responds:

There is consensus that both spinal and epidural anesthesia appear to be safe alternatives for patients with SECONDARY HSV2 infections undergoing labor and vaginal delivery, or for cesarean delivery. However there isn't enough data to make a statement about the safety of neuraxial anesthesia in patients with PRIMARY infection who may be viremic (usually with systemic symptoms like headache, fever, and lymphadenopathy).

Reference:

  1. Wedel DJ. Horlocker TT. Risks of regional anesthesia—infectious, septic. Regional Anesthesia. 21(6 Suppl):57-61, 1996 Nov – Dec.
  2. Bader AM. Camann WR. Datta S. Anesthesia for cesarean delivery in patients with herpes simplex virus type-2 infections. Regional Anesthesia. 15(5):261-3, 1990 Sep – Oct.
  3. Ravindran RS. Gupta CD. Stoops CA. Epidural analgesia in the presence of herpes simplex virus (type 2) infection. Anesthesia & Analgesia. 61(8):714 – 5, 1982 Aug.


I recently encountered a 35-yr-old female undergoing in vitro fertilization under mask inhalation using halothane. During the procedure, the surgeon gave HCG and she had pink, frothy sputum. I had to intubate and care in the ICU for 2 d, after which she was echoed. Nothing was found to explain this event. —kamthorn@health.moph.go.th

Dr. Peter Dwane responds:

Ovarian hyperstimulation syndrome (OHSS) occurs in 1-30 % of women after the induction of ovulation, in the luteal phase of the menstrual cycle. The more frequent occurrence of the disease would be based on inclusion of any mild symptoms of abdominal discomfort and fullness. Most commonly in the mild form, it consists of abdominal discomfort and distension with nausea and/or vomiting. In more severe cases there can be as cites, which can progress to severe dehydration which, in turn, can progress to end organ dysfunction: renal dysfunction, coagulopathy, ARDS. Rarely this syndromecan be fatal.

The etiology of this syndrome in poorly understood but is felt to be due to release of mediators which cause increased vascular permeability with resultant loss of intravascular volume to the interstitial space. The resulting hypovolemia leads to the previously mentioned complications. I have not read of a case of isolated pulmonary edema associated with OHSS, although two cases of isolated pleural effusions have been reportedby WT Gregory (3).

Of course, two anesthetic causes of pulmonary edema would have to be ruledout: aspiration, and negative pressure pulmonary edema form complete airwayobstruction during forceful inspiration.

References:

  1. Beerendonk CC. van Dop PA. Braat DD. Merkus JM. Ovarian hyperstimulation syndrome: facts and fallacies. Obstetrical & Gynecological Survey. 53(7):439-49, 1998 Jul.
  2. Sauer MV. Defining the incidence of serious complications experienced by oocyte donors: a review of 1000 cases. American Journal of Obstetrics & Gynecology. 184(3):277-8, 2001 Feb.
  3. Gregory WT. Patton PE. Isolated pleural effusion in severe ovarian hyperstimulation: A case report. American Journal of Obstetrics & Gynecology. 180(6 Pt 1):1468-71, 1999 Jun.


What is the safest treatment for post surgical n/v emergency anesthetic during the first trimester of pregnancy?—rsilver1@tampabay.rr.com

Dr. Peter Dwane responds:

A major concern with using drugs in pregnancy, especially in the first trimester, is teratogenicity. The incidence of major malformations in the general population is 2-3%, but only 2-3% of these malformations (0.09% of all major malformations) is due to drug effect. This discussion presumes the safest, effective postoperative antiemetics, and therefore excludes common drugs used to treat "morning sickness." Also, proper steps must be taken to prevent postoperative nausea and vomiting (PONV) using appropriate anesthetic techniques, coupled with preoperative medication. Common postoperative antiemetics in this setting would include: ondansetron, droperidol, and metoclopramide. The Food and Drug Administration (FDA) lists five categories (A to D andcategory X) for drugs use in pregnancy. Few drugs are in category A, where controlled human trials fail to demonstrate fetal risk. In both categories B & C there are no controlled human studies that demonstrate human fetal risk. But, in category C drugs, there are animal studies that have demonstrated teratogenicity, while there are no such animal studies with category B drugs. As a result, there is a suggestion that category B drugs may be less likely to cause fetal harm. Practically, both category B & C drugs carry very little risk offetal damage. Most commonly used anesthetic drugs are in categories B & C:

DRUG CATEGORY

  • Ondansetron B
  • Metoclopramide B
  • Propofol B
  • Droperidol C

If there were no differences in drug efficacy, or adverse reactions, between drugs in both categories B & C, I would choose the drug in category B. But if I felt that an antiemetic in category C was more efficacious, or was less likely to cause a significant adverse reaction I would not hesitate to use the category C drug.

References:

  1. Niebyl JR in Drugs in Pregnancy and Lactation: Obstetrics Normal and Problem Pregnancies. Ed: Gab, Niebyl, and Simpson. 3rd Ed. Churchill Livingston, NewYork:1996
  2. Niebyl JR in Nonanesthetic Drugs During Pregnancy and Lactation: Obstetric Anesthesia Principles and Practice. Ed: Chestnut DH. 2nd Ed. Mosby, St. Louis:1999.



Is there any IV agent that will relax the uterus enough for the OB to explore it manually?
— L Mahler LMahler127@aol.com

Dr. Peter Dwane responds

Although I am unaware of a prospective, randomized, control trial which demonstrates the superiority of nitroglycerin (GTN) over other tocolytics (inhaled volatile anesthetics being the gold standard) for ACUTE uterine relaxation for exploration, it has been used for over ten years to achieve uterine relaxation in many situations, and has allowed the avoidance of general anesthesia on countless occasions. This drug can be used both intravenously in doses of 50 to 500 micrograms, and form a metered-dose sublingual spray delivering 400-800 micrograms. The two references below are review articles which may be helpful in summarizing our knowledge to date. GTN has been shown to be an effective tocolytic for premature labor.

References:

  1. Smith GN Brien JF. Use of nitroglycerin for uterine relaxation. [Review] [57 refs]. Obstetrical & Gynecological Survey. 53(9):559-65, 1998 Sep.

  2. Dufour P Vinatier D Puech F. The use of intravenous nitroglycerin for cervico-uterine relaxation: a review of the literature. [Review] [25 refs]. Archives of Gynecology & Obstetrics. 261(1):1-7, 1997.

We recently had a presentation at our M&M conference of a case where an epidural catheter was placed intrathecally. Diagnosis was delayed by a few hours because a test dose was not given through the catheter. The unresolved question at our conference was whether the catheter should have been removed and replaced once the diagnosis was made, or should the catheter have been left in the intrathecal space and used as a continuous spinal anesthetic? Would leaving the catheter in the intrathecal space for a period of time actually reduce the headache incidence in the parturient, and if so, what is a reasonable amount of time?
— D. Newbrun, MD dan1030@flashcom.net

Dr. Peter Dwane responds:

After unintentional dural puncture in the parturient, the incidence of postdural puncture headache (PDPH) is approximately 45% whether the "epidural" catheter is resited as an epidural catheter, or remains subarachnoid as a continuous spinal catheter [1, 2, 4]. Cohen [3] reported a substantial decrease in PDPH in thirteen surgical patients in whom the spinal catheter was used both intraoperatively and for more that 24 hours of postoperative neuraxial analgesia, when compared to a similar group of patients where the catheter was removed at the end of surgery. However this study is small, retrospective and non-randomized.

When considering continuous spinal anesthetic (CSA) one must also remember that

a number of authors [4] have reported an increased incidence of neurological complications after its use. Here again there is uncertainty as to the exact cause (direct catheter effect, specific local anesthetic drug, or local anesthetic concentration) of these problems. Other authors are more supportive of the technique [5-6].

I have used CSA in the setting which you mention. But until we know more about

the neurologic complications of CSA, and their exact causes and incidence, I will reserve the technique for patients who have risk factors that cause me to want to avoid more standard obstetric analgesia/anesthesia practices.

References:

  1. Norris MC, Leighton BL. Continuous spinal anesthesia after unintentional dural puncture in parturients.
    Regional Anesthesia
    1990,15:285-7.
    Click here for abstract

  2. Blaise GA, Cournoyer S, Perrault C, Bedard MJ, Petit F, Landry D. Spinal catheter does not reduce post-dural puncture headache after caesarean section [letter].
    Canadian Journal of Anaesthesia
    1992, 39(6):633-4.

  3. Cohen S, Amar D, Pantuck EJ, Singer N, Divon M. Decreased incidence of headache after accidental dural puncture in caesarean delivery patients receiving continuous postoperative intrathecal analgesia.
    Acta Anaesthesiologica Scandinavica
    1994, 38(7):716-8.

    Click here for abstract

  4. Horlocker TT, McGregor DG, Matsushige DK, Chantigian RC, Schroeder DR, Besse JA. Neurologic complications of 603 consecutive continuous spinal anesthetics using macrocatheter and microcatheter techniques. Anesthesia & Analgesia 1997, 84(5):1063 70.
    Click here for abstract

  5. Lambert DH. Is continuous spinal anesthesia really so bad? Anesthesia & Analgesia 1997, 86:214-5. [letter]

  6. Denny NM, Selander DE. Continuous spinal anaesthesia. Br J Anaesthesia 1998, 81:590-7.[review]

A 25 year old woman was admitted to our hospital for emergency c/s in her first pregnancy due to CPD. There were no problems in her past medical history and physical examination. We chose spinal anesthesia with 1.5 cc lidocaine 5% through L3L4 space and 23G needle after prehydration with 1L ringer. Position was horizontal and left tilt, surgery progressed well until the patient was dyspenic and agitated (15 min after spinal), BP rose from130/80 to 180/110 and PR was 140/min. During the assessment of the patient she complained of breathlessness. During the 45 seconds the patient went into apnea and unconsciousness and double mydriasis, but BP and PR were still the same. She was intubated rapidly without any medications and was hyperventilated with pure oxygen. The newborn was good and didn't need any CPR. Her BP was controlled with nifedipine. After about 45 min the patient gained her consciousness, mydriasis was disappeared and extubated. Post anesthesia course was good. Is total spinal one of the causes of this clinical picture, despite hypertension and tachycardia?
— Dr. Nasser Yeganeh

Dr. Peter D. Dwane responds:

I am at a loss to explain with any certainty what did happen with the patient that you describe.

Firstly, your technique should have resulted in a block to the level of between T8 to T3 which is suitable for a cesarean section, and would cause the patient to have a normal blood pressure. Also the onset of lidocaine block would be of the order of a minute or two, and by 15 minutes the upper level of the spinal block would be "fixed;" that is, it would not extend in a more cranial direction.

It is quite rare to have a very high block or a total spinal with this kind of dose and technique--although this is a possibility.

The symptoms and signs of this whole episode are compatible with a high or total spinal block, except the hypertension and tachycardia, which I am unable to explain. It is my understanding that with a high or total spinal there is not a functional peripheral sympathetic system (at the level of the segmental nerve roots of the spinal cord) to cause vasoconstriction and cardiac stimulation, even if there was some central nervous system reason which could cause the stimulation of brainstem sympathetic centers. In fact, the presence of a relative or absolute bradycardia and hypotension is often seen with total spinal.

An equally uncertain explanation is that there might have been a catechol substance present, either endogenous or exogenous, in origin to explain the hypertension and tachycardia, especially since its severity required treatment with a vasodilator. And this would point to either inadvertent vasopressor drug administration, or to a pheochromocytoma. The hypertensive crisis could have initiated a seizure, accounting for the loss of consciousness, and the return to consciousness, without other permanent sequelae. It would be unusual to not have residual hypertension after this episode and I realize that this is quite a stretch for the imagination. In addition it would be exceedingly fortunate to have not suffered a residual neurological deficit secondary to the hypertensive crisis.

However, I still remain at a loss to explain the hypertension and tachycardia in the face of total sympathetic nervous system blockade.

 



Is there any IV agent that will relax the uterus enough for the OB to explore it manually?
— L Mahler LMahler127@aol.com

Dr. Peter Dwane responds

Although I am unaware of a prospective, randomized, control trial which demonstrates the superiority of nitroglycerin (GTN) over other tocolytics (inhaled volatile anesthetics being the gold standard) for ACUTE uterine relaxation for exploration, it has been used for over ten years to achieve uterine relaxation in many situations, and has allowed the avoidance of general anesthesia on countless occasions. This drug can be used both intravenously in doses of 50 to 500 micrograms, and form a metered-dose sublingual spray delivering 400-800 micrograms. The two references below are review articles which may be helpful in summarizing our knowledge to date. GTN has been shown to be an effective tocolytic for premature labor.

References:

  1. Smith GN Brien JF. Use of nitroglycerin for uterine relaxation. [Review] [57 refs]. Obstetrical & Gynecological Survey. 53(9):559-65, 1998 Sep.

  2. Dufour P Vinatier D Puech F. The use of intravenous nitroglycerin for cervico-uterine relaxation: a review of the literature. [Review] [25 refs]. Archives of Gynecology & Obstetrics. 261(1):1-7, 1997.

We recently had a presentation at our M&M conference of a case where an epidural catheter was placed intrathecally. Diagnosis was delayed by a few hours because a test dose was not given through the catheter. The unresolved question at our conference was whether the catheter should have been removed and replaced once the diagnosis was made, or should the catheter have been left in the intrathecal space and used as a continuous spinal anesthetic? Would leaving the catheter in the intrathecal space for a period of time actually reduce the headache incidence in the parturient, and if so, what is a reasonable amount of time?
— D. Newbrun, MD dan1030@flashcom.net

Dr. Peter Dwane responds:

After unintentional dural puncture in the parturient, the incidence of postdural puncture headache (PDPH) is approximately 45% whether the "epidural" catheter is resited as an epidural catheter, or remains subarachnoid as a continuous spinal catheter [1, 2, 4]. Cohen [3] reported a substantial decrease in PDPH in thirteen surgical patients in whom the spinal catheter was used both intraoperatively and for more that 24 hours of postoperative neuraxial analgesia, when compared to a similar group of patients where the catheter was removed at the end of surgery. However this study is small, retrospective and non-randomized.

When considering continuous spinal anesthetic (CSA) one must also remember that

a number of authors [4] have reported an increased incidence of neurological complications after its use. Here again there is uncertainty as to the exact cause (direct catheter effect, specific local anesthetic drug, or local anesthetic concentration) of these problems. Other authors are more supportive of the technique [5-6].

I have used CSA in the setting which you mention. But until we know more about

the neurologic complications of CSA, and their exact causes and incidence, I will reserve the technique for patients who have risk factors that cause me to want to avoid more standard obstetric analgesia/anesthesia practices.

References:

  1. Norris MC, Leighton BL. Continuous spinal anesthesia after unintentional dural puncture in parturients.
    Regional Anesthesia
    1990,15:285-7.
    Click here for abstract

  2. Blaise GA, Cournoyer S, Perrault C, Bedard MJ, Petit F, Landry D. Spinal catheter does not reduce post-dural puncture headache after caesarean section [letter].
    Canadian Journal of Anaesthesia
    1992, 39(6):633-4.

  3. Cohen S, Amar D, Pantuck EJ, Singer N, Divon M. Decreased incidence of headache after accidental dural puncture in caesarean delivery patients receiving continuous postoperative intrathecal analgesia.
    Acta Anaesthesiologica Scandinavica
    1994, 38(7):716-8.

    Click here for abstract

  4. Horlocker TT, McGregor DG, Matsushige DK, Chantigian RC, Schroeder DR, Besse JA. Neurologic complications of 603 consecutive continuous spinal anesthetics using macrocatheter and microcatheter techniques. Anesthesia & Analgesia 1997, 84(5):1063 70.
    Click here for abstract

  5. Lambert DH. Is continuous spinal anesthesia really so bad? Anesthesia & Analgesia 1997, 86:214-5. [letter]

  6. Denny NM, Selander DE. Continuous spinal anaesthesia. Br J Anaesthesia 1998, 81:590-7.[review]

A 25 year old woman was admitted to our hospital for emergency c/s in her first pregnancy due to CPD. There were no problems in her past medical history and physical examination. We chose spinal anesthesia with 1.5 cc lidocaine 5% through L3L4 space and 23G needle after prehydration with 1L ringer. Position was horizontal and left tilt, surgery progressed well until the patient was dyspenic and agitated (15 min after spinal), BP rose from130/80 to 180/110 and PR was 140/min. During the assessment of the patient she complained of breathlessness. During the 45 seconds the patient went into apnea and unconsciousness and double mydriasis, but BP and PR were still the same. She was intubated rapidly without any medications and was hyperventilated with pure oxygen. The newborn was good and didn't need any CPR. Her BP was controlled with nifedipine. After about 45 min the patient gained her consciousness, mydriasis was disappeared and extubated. Post anesthesia course was good. Is total spinal one of the causes of this clinical picture, despite hypertension and tachycardia?
— Dr. Nasser Yeganeh

Dr. Peter D. Dwane responds:

I am at a loss to explain with any certainty what did happen with the patient that you describe.

Firstly, your technique should have resulted in a block to the level of between T8 to T3 which is suitable for a cesarean section, and would cause the patient to have a normal blood pressure. Also the onset of lidocaine block would be of the order of a minute or two, and by 15 minutes the upper level of the spinal block would be "fixed;" that is, it would not extend in a more cranial direction.

It is quite rare to have a very high block or a total spinal with this kind of dose and technique--although this is a possibility.

The symptoms and signs of this whole episode are compatible with a high or total spinal block, except the hypertension and tachycardia, which I am unable to explain. It is my understanding that with a high or total spinal there is not a functional peripheral sympathetic system (at the level of the segmental nerve roots of the spinal cord) to cause vasoconstriction and cardiac stimulation, even if there was some central nervous system reason which could cause the stimulation of brainstem sympathetic centers. In fact, the presence of a relative or absolute bradycardia and hypotension is often seen with total spinal.

An equally uncertain explanation is that there might have been a catechol substance present, either endogenous or exogenous, in origin to explain the hypertension and tachycardia, especially since its severity required treatment with a vasodilator. And this would point to either inadvertent vasopressor drug administration, or to a pheochromocytoma. The hypertensive crisis could have initiated a seizure, accounting for the loss of consciousness, and the return to consciousness, without other permanent sequelae. It would be unusual to not have residual hypertension after this episode and I realize that this is quite a stretch for the imagination. In addition it would be exceedingly fortunate to have not suffered a residual neurological deficit secondary to the hypertensive crisis.

However, I still remain at a loss to explain the hypertension and tachycardia in the face of total sympathetic nervous system blockade



A 25 year old woman was admitted to our hospital for emergency c/s in her first pregnancy due to CPD. There were no problems in her past medical history and physical examination. We chose spinal anesthesia with 1.5 cc lidocaine 5% through L3L4 space and 23G needle after prehydration with 1L ringer. Position was horizontal and left tilt, surgery progressed well until the patient was dyspenic and agitated (15 min after spinal), BP rose from130/80 to 180/110 and PR was 140/min. During the assessment of the patient she complained of breathlessness. During the 45 seconds the patient went into apnea and unconsciousness and double mydriasis, but BP and PR were still the same. She was intubated rapidly without any medications and was hyperventilated with pure oxygen. The newborn was good and didn't need any CPR. Her BP was controlled with nifedipine. After about 45 min the patient gained her consciousness, mydriasis was disappeared and extubated. Post anesthesia course was good. Is total spinal one of the causes of this clinical picture, despite hypertension and tachycardia? — Dr. Nasser Yeganeh

Dr. Peter D. Dwane responds:

I am at a loss to explain with any certainty what did happen with the patient that you describe.

Firstly, your technique should have resulted in a block to the level of between T8 to T3 which is suitable for a cesarean section, and would cause the patient to have a normal blood pressure. Also the onset of lidocaine block would be of the order of a minute or two, and by 15 minutes the upper level of the spinal block would be "fixed;" that is, it would not extend in a more cranial direction.

It is quite rare to have a very high block or a total spinal with this kind of dose and technique--although this is a possibility.

The symptoms and signs of this whole episode are compatible with a high or total spinal block, except the hypertension and tachycardia, which I am unable to explain. It is my understanding that with a high or total spinal there is not a functional peripheral sympathetic system (at the level of the segmental nerve roots of the spinal cord) to cause vasoconstriction and cardiac stimulation, even if there was some central nervous system reason which could cause the stimulation of brainstem sympathetic centers. In fact, the presence of a relative or absolute bradycardia and hypotension is often seen with total spinal.

An equally uncertain explanation is that there might have been a catechol substance present, either endogenous or exogenous, in origin to explain the hypertension and tachycardia, especially since its severity required treatment with a vasodilator. And this would point to either inadvertent vasopressor drug administration, or to a pheochromocytoma. The hypertensive crisis could have initiated a seizure, accounting for the loss of consciousness, and the return to consciousness, without other permanent sequelae. It would be unusual to not have residual hypertension after this episode and I realize that this is quite a stretch for the imagination. In addition it would be exceedingly fortunate to have not suffered a residual neurological deficit secondary to the hypertensive crisis.

However, I still remain at a loss to explain the hypertension and tachycardia in the face of total sympathetic nervous system blockade.



How useful is epispinal in Obstetrical anesthesia or Gynecological anesthesia for procedures such as c-sections or hysterectomies (either abdominal or vaginal). — Dr. Soundappan

Dr. Peter D. Dwane responds:

Spinals and epidural anesthesia have been used for many decades for operative Obstetrics and Gynecological surgery. Initially, spinals were limited to older patients because of the fear of postdural puncture headache. But with the advent of the smaller, pencil point needles even young pregnant patients have become candidates for spinals.

In the last 5-7 years, combined spinal-epidurals (CSEs) have frequently been used in obstetrics. Several institutions use the CSE as their analgesia of choice for the majority of laboring women. Personally, I reserve it for patients whom I expect will deliver before the spinal part of the CSE subsides (usually 90 minutes), that is multiparas laboring well, and at more than 7 cm dilation.

The CSE can be used for surgery, where the spinal phase is used for its low failure rate and excellent block, while the epidural catheter is left in place as "insurance" to extend the spinal block either spatially or temporally; and then to handle the postoperative analgesia. With this technique (CSE) I have started to use isobaric bupivacaine for the spinal phase, when I want the block to extent up to the second to fourth thoracic dermatome. However, with Gynecological surgery "heavy" bupivacaine via the spinal needle would be fine. CSEs are excellent to use for many GYN surgeries of less than three hours.



A 25 y.o. lady came for normal delivery of a full term female baby. An epidural was sited which was working well. After an uneventful delivery, the mother started to complain of headache next morning on sitting up. She was tried first with oral fluids (3 L per day) and analgesics, and blood patch was planned after 48 hours. However, early in that morning she awoke with severe neck pain which did not respond to analgesics and she experienced fits which were controlled with diazepam and epanutin infusion. Her CT showed that she suffered from a right tempro-pareital haemorrhagic infarction. MRI confirmed this and an MRA showed that there was no sinus thrombosis. Could a dural tap be the cause? Or it might be a late picture of eclampsia? (Note: This young lady did not suffer from any abnormalities whatsoeverBP and all other data were normal all through these events.)   -- R. Ramzy

Dr. Dwane Responds:
I can think of no mechanism whereby a dural puncture can cause a haemorrhagic infarct, unless there were a preexisting lesion in that area of the patients brain.



A patient at high risk for Huntington's Disease (HD)is scheduled for two ophthalmic procedures under general anesthesia. Her neurological and physical status is strictly normal, but her risk of HD was determined by family history and genetic analysis (42 triplets). Is it possible that these two non-vital procedures under general anesthesia could trigger an HD in the postoperative period? On the other hand, could these procedures interfere with the natural course of HD in an at-risk patient?   -- P. Hoffreumon, M.D.

Dr. Dwane Responds:
To my knowledge, the usual anesthetic drugs do not affect the onset or course of Huntington's Disease.



I have been using Pontocaine (tetracaine) for spinal regional anesthesia for the past 10-plus years, especially for cesarean section and other uncomplicated surgeries. Why do so many anesthetists want to use other local agents than Pontocaine? Why are most or almost all anesthesiologists are avoiding use of Pontocaine for spinal anesthesia? Cost, long acting, side effects? What is the future of Pontocaine?   -- Joe Haleyalmang

Dr. Dwane Responds:
Tetracaine is an "older" anesthetic which has been used for years for spinal anesthetics. For a longer acting anesthetic, it has always worked as well as any other available agent. Since the recent concern about transient neuroradiculopathy with 5% hyperbaric lidocaine, bupivacaine and tetracaine are the two commonly used "safe" anesthetics used for spinals.

Because tetracaine is commonly available as a powder, it must be reconstituted with either CSF or sterile water, and then mixed with 10% dextrose to obtain the desired baricity before use. I suspect that many anesthesiologists prefer to crack an amp of a ready-mixed drug like bupivacaine—no worries about correct dilution, and no fuss or muss with mixing stuff, just instant gratification!... Not cost, complications, or duration.

I used tetracaine for 15 years before switching to bupivacaine, only because it was "more modern". I'm lazy too. For the past ten years, I haven't seen much difference between bupivacaine and tetracaine except the convenience of a premixed drug. In fact, at the large hospital where I now practice, our spinal kits come with powdered tetracaine and most of my colleagues still add an amp of 0.75% "heavy bupivacaine" to the setup too!



We recently had a group of midwives join our obstetrical department. Our current policy is to have an obstetrician on campus whenever we institute a continuous epidural anesthetic. What are your thoughts on instituting an continuous epidural with just the midwife present and an obstetrician immediately available (10-15 minutes)?   -- Dr. Jeffrey A. Haiken

Dr. Dwane Responds:
Firstly:
The ASA guidelines for regional anesthesia in obstetrics (1991; no. 3) states that an epidural may be administered after the patient has been examined by a qualified person; and the maternal and fetal status and progress of labor has been evaluated by a physician with privileges in obstetrics who is readily available...

Also, in the new ASA draft of practice guidelines for obstetric anesthesia there is no mention of these limitations.

I do not see any impediment to providing epidural analgesia to a patient who has been evaluated by a physician with obstetric privileges. Realizing the political overtones, the midwives would need to come to an arrangement with an obstetrician or obstetric group to "cover" patients evaluated by midwives. Once this agreement is in place then it would be appropriate to provide analgesia service to the laboring mom.

Without this obstetrician evaluation, I am uncertain of the legal standing of an anesthesiologist functioning under the sole direction of a midwife.

Secondly:
If the obstetrician is available to intervene within 10 - 15 minutes, this is well within the 30 minutes necessary for an obstetric unit to be able to mount a Cesarean Section.



Perioperative fetal monitoring in non-obstetric surgery has become more common. A recent article states that 60% of responding hospitals use it. I can find no guidelines or protocols to help us in developing one for use in our private hospital. Specifically, we do not have in-house obstetrical surgeons: What is the required availability for a trained surgeon to deal with fetal distress (4-5 minutes is recommended if the mother arrests - ACLS guidelines)? Which patients should be monitored? All pregnant patients? or just those over 25 weeks where fetal viability is an issue? Is there any literature or data to prove that monitoring is of any benefit?   -- Kenneth L. Bachenberg, M.D.

Dr. Dwane Responds:

1) An obstetrical unit must be able to mount a Cesarean Section within 30 minutes of the identified need.
2) Several Anesthesia textbooks, as well as Obstetric Anesthesia texts and the ASA annual refresher course lectures on the subject for the last four years, recommend intraoperative fetal monitoring after 16-20 weeks gestation, but none of these statements are referenced with regard to the efficacy of the recommended practice. They do stress that this monitor is used to check on inadvertent changes that might affect intraoperative placental perfusion and oxygenation.

Fetal heart rate monitoring in the preoperative setting is used to identify :
A) Material conditions which might require optimization: blood pressure, oxygenation, hemoglobin concentration, temperature, position, surgical interference with inadequate uterine perfusion. This is not the usual fetal heart (FH) monitoring done during labor to decide whether or not to intervene in the labor process.
B) The onset of premature labor, usually in the PACU or postoperative ward, so that tocolysis may be instituted should the obstetrician deem it appropriate.

  • Fetal monitoring is not mentioned in the ASA Standards For Basic Anesthetic Monitoring.
  • Fetal heart rate variably is present by about the 25th week of gestation and can be affected by anesthetic drugs.
  • Prolonged fetal bradycardia is usually indicative of true fetal distress.
  • Fetal monitoring may be technically difficult/impossible with certain surgeries.
  • As well as a qualified person to interpret the FH tracing in real time in the operating room, a plan of action based on the potential FH tracing changes must be in place beforehand (established by the Obstetric group).
Having said all this, I am not aware of randomized, blinded trials that have looked at the efficacy of FH monitoring during surgery. There are many papers reporting successful post-surgical fetal outcomes, but often the fetus is less than 20 weeks gestation and/or fetal monitoring is not used intraoperatively.

Your options as I see it are:
A) To not under take fetal monitoring (as do 40% of hospitals in the survey you cite).
B) Refer pregnant patients requiring surgery to a facility with a responsive obstetric service.
C) Request the obstetrician(s) who would ultimately decide (from the clinical situation and the fetal heart rate tracing) that a C/Section is or is not necessary to set up an appropriate protocol.




I recently gave anesthesia for a repeat Cesarian Section patient who went into labor one day prior to her scheduled OR date. Thank Heaven she asked for a spinal, because her complaints (chest tightness, SOB, heart pounding, HA, consistent coughing) told us something was wrong before her O2 sat. changed (never below 94%). She also developed a 2nd degree heart block which was treated with 1mg atropine; her HR rose from 50's to 190's and her BP went up to 190/110 (from unmeasurable by NIBP). She remained alert and breathing, and was taken postoperatively to our ICU with O2 sat. 95% on 4L O2. All complaints except coughing had disappeared, but ABG's showed hypoxia and hyperventilation. SBP was 100's, HR 100's (sinus tach). She was flown from our small, rural hospital to a larger regional center for suspected amniotic fluid embolus, which was confirmed (V/Q scan etc. although I don't have all the details). She had a mild bout of DIC, but two weeks later seems to have recovered (except for a platelet count of approx. 100,000).

I am currently exploring textbooks and reviewing published literature regarding this type of event. Have any of your experts had a case like this? How might this case have presented itself had the patient had general anesthesia? Do you have any references you feel are particularly helpful?   -- Jackie Marfilius, CRNA

Dr. Dwane Responds:
Current articles on Amniotic Fluid Embolism (AFE) deal with the more conventional picture: sudden onset of respiratory distress, hypoxemia, and, cardiovascular collapse, often with DIC, and occasionally presenting as a seizure. Often, 1/3 of patients die within the first 2 hours after clinical presentation, and another 1/3 die over the next 3 hour period. The syndrome of AFE is difficult to confirm even in its severe form, especially without autopsy results.

Your patient seems to have had a much milder form of the disease, which I have not encountered. However the initial hypertensive response may be similar to that seen in an experimental goat model reported by G.D.U. Hankins in 1993.

I suspect that under general anesthesia the presentation of AFE in your patient would have been similar hypoxemia, EKG change, and hypertension. As the occurrence was mild there is no evidence of myocardial dispersion or profound hypoxemia, and thus no cardiovascular collapse.

S.L. Clark et al and R.J. McDougall et al present current reviews on the topic - see references. The last two references I included to argue that minor air embolism, commonly seen with doppler monitoring at C/Section does not present a picture similar to that seen in your patient.

References:
1. Clark SL. Hankins GD. Dudley DA. Dildy GA. Porter TF. Amniotic fluid embolism: analysis of the national registry [see comments].Am J Obstet Gynecol 1996 Sep;175(3 Pt 1):749

2. McDougall RJ. Duke GJ. Amniotic fluid embolism syndrome: case report and review.Anaesthesia & Intensive Care. 23(6):735-40, 1995 Dec.

3. Fong J. Gadalla F. Pierri MK. Druzin M. Are Doppler-detected venous emboli during cesarean section air emboli? Anesthesia & Analgesia. 71(3):254-7, 1990 Sept.

4. Handler JS. Bromage PR. Venous air embolism during cesarean delivery. Regional Anesthesia. 15(4):170-3, 1990 Jul-Aug.



I was recently at a presentation on "Anesthesia for Obstetric Emergencies". The speaker suggested using intravenous nitroglycerine for profound uterine relaxation. The benefits included avoiding general anesthesia and a short duration of action. In her experience she saw no clinically significant decreases in blood pressure, such as with halothane, and NTG had a much shorter duration of action as compared to terbutaline. The specifics she gave were starting with a dose of 50-100 micrograms and repeating that dose every one minute. Onset should be 30-90 seconds, with a duration of 2-3 minutes. Repeat dosing to a maximum of 500 micrograms. I work in a small town hospital with an active OB department. One of my colleagues used this technique recently for a retained placenta and it worked great. We are interested in writing a protocol for the use of NTG for uterine relaxtion in emergency situations when anesthesia is not immediatly available. This would give the family practice physicians and OB nurses and extra tool to deal with specific OB emergencies while anesthesia is on the way. I have done a literature search and been unable to find specific documentation on dose, route, duration etc. to back up the presentation I attended. Also, I would be interested in situations that your experts have seen this used.   -- Debra Drew CRNA

Dr. Dwane Responds:
Although no randomized controlled trials have documented the efficacy and safety of GTN for provision of uterine relaxation, IV GTN has been used for more than 8 years to provide uterine relaxation. In Dr. Chestnut's book, Obstetric Anesthesia Principles and Practice, P. 711, he mentions single bolus doses of 50 - 500 micrograms and comments that 500 micrograms may be excessive (see references provided).

Basically the data you present is sound. However, I would point out that the doses used require dilution of the drug as it is supplied by the pharmacy (in either 50 or 5 milligram/ml concentration therefore 50,000 or 5,000 microgram/ml concentration). You can see where an error in calculation, or in dilution technique can result in an enormous over dose. Many patients have either died or come to harm by Anesthesiologists, CRNAs, and Surgeons miscalculating drug dilutions - e.g. epinephrine and MgSO4.

I recommend for non-anesthesia personnel that sublingual nitroglycerine spray 0.4 mg (400 microgram metered dose) might be a reasonable substitute for the more precise, but more risk prone dilution of unfamiliar drugs in an emergency (see references 1 & 2 by Dr. E. Bell).

References:
1. Bell E. Nitroglycerin and uterine relaxation [letter] [see comments].Comment in: Anesthesiology 1997 Sep;87(3):716-7

2. Redick LF. Livingston E. Bell E. Sublingual aerosol nitroglycerin for uterine relaxation in attempted external version [letter]. American Journal of Obstetrics & Gynecology. 176(2):496-7, 1997 Feb.

3. Lowenwirt IP. Zauk RM. Handwerker SM. Safety of intravenous glyceryl trinitrate in management of retained placenta. Australian & New Zealand Journal of Obstetrics & Gynaecology. 37(1):20-4, 1997 Feb.

4. Chan AS. Ananthanarayan C. Rolbin SH. Alternating nitroglycerin and syntocinon to facilitate uterine exploration and removal of an adherent placenta. Canadian Journal of Anaesthesia. 42(4):335-7, 1995 Apr.



Is there literature to support the use of propofol for use in pregnant patients having general anesthesia for c-section or in pregnant patients having non-OB/gyn procedures under general anesthesia?   -- Worktoeat

Dr. Dwane Responds:
The answer to both questions is "yes". See attached references taken from a list of 32 that I could find published since 1989.

However, Zeneca Pharm cautions in its propofol drug insert that the drug "should be used during pregnancy only if clearly needed," that it is "not recommended for obstetrics, including cesarean section deliveries," and it is "not recommended for use in nursing mothers". This means that medicolegally you could be on the defensive, having to prove that the use of propofol meets current standards of practice.

I would ask what you're trying to achieve that you don't achieve with thiopental, aside from avoiding the barbiturate's increased incidence of nausea and vomiting. Propofol may bring with it a greater duration of apnea after an induction dose should a difficult airway surprise you. In addition, maternal bradycardia has been seen in sheep with inductions using propofol and succinylcholine, as you might for a rapid-sequence induction.

I will concede that some anesthesiologists use propofol with pregnant patients.

Selected Propofol & Pregnancy References:
Rosenblatt MA, Bradford CN, Bodian CA, Grunfeld L. The effect of a propofol-based sedation technique on cumulative embryo scores, clinical pregnancy rates, and implantation rates in patients undergoing embryo transfers with donor oocytes. J Clin Anesth. 1997;9(8):614-7.

Hein HA, Putman JM. Is propofol a proper proposition for reproductive procedures? [editorial]. J Clin Anesth. 1997;9(8):611-3.

Abboud TK, Zhu J, Richardson M, Peres Da Silva E, Donovan M. Intravenous propofol vs thiamylal-isoflurane for caesarean section, comparative maternal and neonatal effects. Acta Anaesthesiologica Scandinavica. 1995;39(2):205-9.

Vincent RD Jr, Syrop CH, Van Voorhis BJ, Chestnut DH, Sparks AE, McGrath JM, Choi WW, Bates JN, Penning DH. An evaluation of the effect of anesthetic technique on reproductive success after laparoscopic pronuclear stage transfer. Propofol/nitrous oxide versusisoflurane/nitrous oxide. Anesthesiology. 1995;82(2):352-8.

Gin T, O'Meara ME, Kan AF, Leung RK, Tan P, Yau G. Plasma catecholamines and neonatal condition after induction of anaesthesia with propofol or thiopentone at caesarean section. Br J Anaesth. 1993;70(3):311-6.

Celleno D, Capogna G, Emanuelli M, Varrassi G, Muratori F, Costantino P, Sebastiani M. Which induction drug for cesarean section? A comparison of thiopental sodium, propofol, and midazolam. J Clin Anesth. 1993;5(4):284-8.


An obstetric colleuge of mine is under the impression that a labor epidural's local anesthetic can diminsh or abolish utererine contractions by acting as a smooth muscle relaxant. We obviously disagree on this point. He will commonly request that the epidural infusion be turned down or off to allow the uterus "to recover" when a parturiants labor stalls! As you can imagine this undermines a patients confidence in her anesthesiologist and labor epidurals when her obstitrican implies the epidural has caused her labor to stall despite our explanation otherwise. Do you know of such an effect? My own liturature search has proved fruitless.   -- Jeffrey Reed, MD

Dr. Lubarsky Responds:

There is no effect of local anesthetics on smooth muscle. Period.

As to stalling labor, well, there is some controversial evidence that labor will slow when the epidural is placed very early in labor, but the effect is small. If you are placing the epidural during active labor, and using dilute local anesthetics, there is little likelihood of any effect on the progress of labor.




I would like to know your opinion on the use of "deep MAC" anesthesia with the use of remifentanyl infusion plus propofol infusion for cervical cerclage. This question came up in my practice, and as you might well imagine there were conflicting opinions on the use of this technique,i.e., endotracheal intubation vs. a deeply sedated, spontaneously breathing patient. In giving your response, please consider the fact that the patient does retain spontaneous respirations throughout the procedure with the use of the above mentioned technique.   -- G. Hartzog, CRNA

Dr. Philip Responds:

The answer to your question depends on whether "deep MAC" is an appropriate anesthetic type for the patient's stage of pregnancy. In mid-pregnancy and beyond, the concern is regurgitation and aspiration, and non-intubated general anesthesia techniques are not appropriate. Whether an anesthetic is MAC or General does NOT depend on whether the patient is breathing spontaneously; rather it depends on whether the patietn retains all protective reflexes. If in this "deep Mac" technique, the patient can no longer repsond purposefully to noxious stimuli -- is unresponsive to surgical stimuli--, that IS intravenous general anesthesia, and requires endotracheal anesthesia and full-stomach precaustions. In our institution, spinal anesthesia is definitely the preferred technique.
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