Nausea and vomiting (NV) is an unpleasant and sometime dangerous side effect during C-section (CS). In our article we will consider only those cases done under spinal and epidural anesthesia. We are excluding cases done under general anesthesia because intubated and anesthetized patients cannot feel nausea and the main concern is risk of aspiration. Post operative NV (PONV) has different causes and risk factors. Treatments have been described extensively elsewhere, and different options have been offered for PONV treatment.
Our main concern and focus in this article will be the role of the vagus nerve in intraoperative NV (IONV). We feel it has not been addressed sufficiently in obstetric anesthesia and effective solutions were not found.Two separate neuronal pathways of sensation from the uterus to the brain, through the spinal cord and vagus nerve(Figure 1) exist and are independent from one from other. Spinal or epidural anesthesia cannot possibly block the vagus nerve, so theoretically (and through our own practice), the full comfort of the patient during C-section under solely spinal or epidural anesthesia is not possible. If we are striving for perfection and trying to provide the best possible care for our patients, the role of the vagus nerve should be addressed. At the present time the only effective way to block undesirable effects of vagus nerve stimulation is sedation. We are glad to report that after recognition of the role of the vagus nerve in generating IONV, we have introduced the concept of mild sedation after delivery. Our rate of IONV during C-section is close to zero.
Materials and Methods
Our retrospective study was approved by IRB. All patients gave consent for anesthesia for scheduled C-section. We will describe the CSE technique that we use in our institution. Wealso place an epidural catheter for post-op pain management, giving epidural morphine for 3 days 2mg twice a day. Small variations in regional anesthesia techniques between institutions arenot relevant in our discussion because none of them cover vagus nerve involvement. We willdescribe our technique in detail to eliminate possible questions as to why an epidural catheter is placed routinely for CS. Patients are in a sitting position with anesthesia monitors in place. Propofol is given IV in small incremental doses 5-10 mg (60mg max) per minute until thedesirable level of sedation is reached. We find this practice reduces anxiety, which helps theanesthesiologist by providing a more comfortable patient. One person is designated to supportthe sedated patient. We ask the patient if she is comfortable and relaxed. Chlorhexedine is used for prep. Local 5ml 2% lidocaine is injected subcutaneously in lumbar area at the L4-L5 level. Patients usually do not react to this or remember the injection. A 17 gauge Touhy needle isplaced in the epidural space using loss of resistance technique. A 27 gauge Whitacre needle is placed through the epidural needle. After witnessing flow of CSF through the spinal needle, 1.2ml of 0.75% Bupivacaine is injected intrathecally. A 19 gauge wired epidural catheter is thenplaced through the epidural needle and is taped, leaving 6 cm of catheter in the epidural space. Patients are placed in the Trendelenburg position without left uterine displacement (LUD). The level of spinal block is usually around T4. 2 mg morphine is given through the epidural catheter after delivery. The patient is usually alert after CSE placement.
Analysis of the course of standard C-section done under spinal, epidural or CSE, revealed three different situations when the patient may feel nauseous and thus vomit.
1) Too rapid administration of antibiotics, usually Ancef (Cefazolin) 2 g. Given IV push, it may cause IONV.
Possible solution: administer antibiotics in 100 ml of NS, IVPB. Another option we found effective is slight sedation of the patient. Some clinicians may find it excessive, but in our practice we sedate the patient for CSE placement on regular basis. We have found that if thepatient is mildly sedated, Ancef can be given IV push without causing IONV. We usually use Propofol for this purpose, titrated to effect. From the moment of sedation until delivery takes approximately 30 minutes. Propofol is eliminated by that time. The patient is awake at delivery,and the baby is not sleepy.
2) IONV caused by hypotension secondary to spinal anesthesia.
The recommended level of spinal block for C-section is T4 . Sympathetic thoracic chain is located in T5-T10 segments and is usually blocked by spinal block up to the T4 level. It causes vasodilatation and profound hypotension.
Possible solution: Vasodilatation is treated by vasoconstriction. Early and aggressive prophylactic administration of Phenylephrine in increments prevents hypotension from developing. We use a technique based on heart rate .We do not use pump. Some authors recommend LUD to prevent aorto venous compression. In our practice, we find that administration of Phenylephrine usually solves the problem and LUD is not necessary. Ephedrine could be used if patient is bradycardic as it fits into our management, based on heart rate.
3) IONV caused by surgeon, during manipulation of the uterus and other internal organs after delivery. Even with strong and adequate spinal block, the patient may complain not only ofIONV but also the sensation of unpleasant pressure and/or shoulder and chest pain. We suggest that it is caused by the stimulation of the vagus nerve. Further discussion are in the “Results and Discussion” section.
Possible solution: Sedation of the patient until she is comfortable. We use a combination of Versed, Propofol and/or Fentanyl, titrated to the effect. The vagus nerve leaves the brain on the medullary level . To block the vagus nerve on this level is practically impossible as regional blocks would be too cumbersome and invasive. In order to be nauseous in most cases, the patient has to be awake. Slight sedation of the patient will not prevent impulses from stimulation of the vagus nerve by the surgeon reaching the medulla, but it will prevent IONV from happening. As we mentioned earlier, introduction of sedation after delivery nearly eliminated IONV in our practice.
Results and Discussion
After reflecting on the problem of IONV during C-section, identifying three main causes of IONV, and by applying the above mentioned methods of solution, we have nearly eliminated IONV during C-sections in our practice. In reviewing the literature on IONV relevant to our situation, we noticed that discussions usually focus on the anatomy of the vomiting center, different types of receptors, and different type of anti-emetic medications. Observation was made that “none of the antiemetic medications are entirely effective”(6).
Taking everything into consideration, we went further by investigating the immediate causes of three types of IONV. All three types develop very rapidly. Zofran, the quickest-working anti-emetic takes up to 20 minutes to take effect making anti-emetic medicationsineffective during C-sections.
Another important point was made clear. In order to be nauseous, the patient needs to be awake. The same concept is applied to shivering. A sedated patent has no NV and does not shiver. The role of the cerebral cortex seems to be of major importance in generating IONV and shivering. Humans do not shiver during sleep. Any rule has exceptions but understanding this concept helped us to find a useful solution.
We understand that the principle of treating IONV with sedation is somewhat controversial in eyes of the modern obstetric anesthesiologist . Anesthesiologists usually resist sedation on a patient with nausea in order to avoid aspiration, a nightmare for both the anesthesiologist and patient. All women that present for C-section are treated as full-stomach patients because of delayed gastric emptying. It is one of the reasons we try to avoid GA. Understanding and applying here our hypothesis that sedated patients do not get nauseous , mild sedation in this light diminishes risk of vomiting and aspiration, and practically prevents vomiting , and as consequence aspiration too.
Role of the vagus nerve
Our hypothesis is that the third type of IONV is caused by the surgeon manipulating the uterus which stimulates the unblocked vagus nerve. Observing our patients during C-sectionsunder CSE, we have noticed that even with an adequate spinal block at the T4 level and no pain upon surgical incision, many women still report nausea, chest and shoulder pain, visceral pain (7,8)and may vomit. These symptoms are especially strong when the uterus is manipulated or exteriorized. These vague unpleasant sensations cannot be propagated through the spinal cord when it is blocked up to the T4 level(Figure1). It cannot be the hypogastric nerve that enters the spinal cord at the T10-T12 level. Referred pain could be transmitted through phrenic nerve that enters spinal cord at C3-C5 (Figure 2).A possible explanation is the existence of the afferent pathway that bypasses the spinal cord through the vagus nerve. This has been shown via multiple elegant experiments on females with damaged spinal cords and on animals with damaged spinal cords by Komisaruk.
Komisaruk (1)showed “(1) Genitospinal visceral afferent pathways function in the women in the group with upper SCI, and/or (2) there exists a functional genital afferent pathway that bypasses the spinal cord and projects directly to the brain, which we propose to be via the vagus nerve.”
Komisaruk (2)proved the existence of this pathway with the vagus nerve role in humans using MRI: ”We conclude that the vagus nerve provides a spinal cord-bypass pathway for vaginal-cervical sensibility in women with complete spinal cord injury above the level of entry into spinal cord of the known genitospinal nerve” and using brain (PET) responses ”These preliminary findings suggest that the vagus nerve can convey genital sensory input directly to the brain in women, completely bypassing SCI at any level” (3).
Komisaruk proved his data with experiments on rats: ”These findings provide evidence that, in the rat, the vagus nerve provide a functional sensory pathway from the reproductive tract directly to the medulla oblongata of the brain, bypassing the spinal cord” Komisaruk (4).
We offer hypothesis that if pleasant stimuli could be transferred through vagus neural pathway, stimuli responsible for visceral and IONV could be transferred too.
These data leads us to the conclusion that two ways of propagation of neural stimuli exist between uterus and brain. One is through the spinal cord and another is through the vagus nerve. We hypothesize that stimulation of the vagus nerve by manipulation of the uterus may play a role in the development of IONV and referred chest and shoulder pain. Both the spinal and vagus pathways should be blocked during C-section. If not, full comfort of the patient is unachievable.The patient could be fully comfortable under spinal anesthesia if the procedure involves organs not innervated by the vagus – for example hip or knee surgeries. We propose slight sedation as an effective means to block the effects of vagus nerve stimulation by manipulation of the uterus. Regional blocks of the vagus nerve would be too invasive and is not practical.
Another situation where vagus nerve involvement can play a role is in post C-section pain management. In our institution, we leave the epidural catheter in for three days and administer morphing 2mg twice a day. Even considering that neuraxial opioids are the “gold standard” for post C-section pain relief, patients may still complain about cramping and gas pains. Epidural morphine works predominantly on the spinal level and does not affect the vagus nerve. Medications that can cover the vagus nerve should be used. We usually give Ketorolac 30 mg or Fentanyl 50 mcg IV. These facts support our theory of vagus nerve involvement.
Full stomach concerns and possible aspiration may be addressed in this way. There issignificant difference between GA and slight sedation. During GA patient has no laryngeal reflexes and is prone to aspiration, but during slight sedation laryngeal reflexes are intact and patient may be kept arousable and responsive. If vomiting occurs, it is very unlikely that the patient will aspirate.
Item for discussion: Effect of sedation on the baby. It usually takes about 30 minutes from the time of last dose of Propofol until the delivery. By that time, sedative effect of Propofol is worn off, and the mother is fully awake as is the baby.
Item for discussion: Effect of sedation on mother-baby bonding. The baby can be shown to the mother immediately after delivery and then small incremental doses of Propofol are given.
Our most important findings during our retrospective study were:
1)First part of our hypothesis- there exist neural pathway for visceral abdominal pain and feeling of nausea and vomiting.This pathway bypasses T4 level of spinal block for csection.It includes vagus nerve and phrenic nerve (Fugures 1 and 2). Role of this pathway and need to block it for full comfort of the patient is underestimated or not addressed at all in literature and practice of obstetric anesthesia.Realization that adequate spinal block of any clinically safe level cannot guarantee complete comfort of the patient. The vagus nerve bypasses the spinal cord completely. In order to block this effect the patient needs to be sedated.
2)Second part of our central hypothesis-sedation prevents nausea , vomiting and vesceral abdominal pain. The realization that in most cases, awake patients are susceptible to IONV and vesceral pain and slight sedation will resolve it.
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