If you wish to respond to a paper or other item already published in the BJA, please go to the abstract/full text version of that item and click on the link "E-Letters: Submit a response to the article".
Electronic Letters to:
|
|
E-letters: Electronic letters published:
-
![[Read E-letter]](/icons/misc/sectionDOWN.gif)
Response to - Really laryngospasm or simply decreased cerebral perfusion?
- Kandasamy Subramani (28 December 2005)
-
Really laryngospasm or simply decreased cerebral perfusion?
- Aysenur Boztepe, Gulcan Berkel Yıldırım (8 December 2005)
-
Re: Laryngospasm during subarachnoid block
- Kandasamy Subramani (19 October 2005)
-
Laryngospasm during subarachnoid block
- Mahindra G Chincholkar (28 April 2005)
|
|
|||
|
Kandasamy Subramani, Consultant Anaesthetist (Currently) Weston General Hospital, Weston-Super-Mare, UK
Send letter to journal:
|
We thank Drs. A.Boztepe G.B.Yıldırım for their interest in our case report. We administered only 2 mgs of midazolam and not 5 mgs as the authors have mentioned. We postulated that the hypovolemia was both actual due to prolonged starvation on a very hot summer day and relative due to vaso-dialatation induced by spinal anesthetic. We had every intention to give IV fluids as the subarachnoid block was being instituted, but did not succeed. The patient was lying on the right lateral side and the drip was on the right arm and hence the fluids did not flow. The patient woke up with laryngospasm and signalled to us that he was not able to breathe. This demonstrates that though the recorded systemic blood pressure was low, the compensatory mechanism to maintain cerebral perfusion was intact. It is also a proof that we did not administer an “overzealous dose of sedatives” as the authors of the letter have interpreted. Moreover, the authors suggest that there could have been a reduced perfusion of respiratory centre due to the low blood pressure which caused laryngospasm. This in our opinion should cause disorders in the respiratory rhythm and not laryngospasm. The laryngospasm was not relieved in 15 seconds as the authors have mentioned. We are sorry if this was not clear in our case report. The laryngospasm took almost three minutes from the time of onset. Could I request the authors to read the case report(1) and my response(2) to a letter to the editor(3) in a later issue of this journal please? It is practically difficult to administer IV fluids, atropine and ephedrine in 15 seconds. Moreover the drugs would take a longer than 15 seconds to be delivered to their site of action in a state of cardiovascular collapse. By reporting our case, our intention was to present an unusual presentation of vagotonia due to hypovolemia, which was managed with vagolytic measures namely atropine, intravenous fluids and ephedrine. Atropine is a direct vagolytic. Hypovolemia was corrected with intravenous fluids and vasoconstriction due to ephedrine and these interventions were vagolytic in our opinion. Laryngospasm during spinal anaesthetic has not been reported for 107 years since the German surgeon, Karl August Bier gave the first spinal anaesthetic in 1898. There may have been similar episodes which were not reported. We expected more questions and alternative theories for the laryngospasm from readers than the two so far! Subramani References 1 Subramani K, Paul A. Laryngospasm during subarachnoid block. Br J Anaesth 2005; 94: 668-70. 2 Subramani K. Laryngospasm during subarachnoid block. Br J Anaesth 2006; 96: 141. 3 Chincholkar MG. Laryngospasm during subarachnoid block. Br J Anaesth 2005; 95: 277. Conflict of Interest:None declared |
|||
|
|
|||
|
Aysenur Boztepe, Anaesthesiologist Kartal Dr. Lutfi Kırdar Training and Research Hospital, Istanbul,Turkey, Gulcan Berkel Yıldırım
Send letter to journal:
|
Editor-Any patient who is given a beta blocker, diazepam 10 mg, midazolam 5 mg, only 100 ml of i.v. fluids after 14 hours of fasting, followed by intrathecal bupivacaine is doomed for serious hypotension. Blood pressure was 70/30 mmHg, which would mean a mean arterial pressure (MAP) of 43 mmHg. Did the author not consider the possibility that such a drop in MAP would result in a decrease in cerebral perfusion with resultant depression of the respiratory center? Loss of pharyngeal muscle tone brought on by the administration of diazepam and midazolam may have contributed by causing upper airway obstruction. The patient’s symptoms were resolved in 10-15 seconds following the administration of i.v. fluids, atropine and ephedrine. Does the author mean that laryngospasm cleared 15 seconds after administration of atropine and hence the assumption that since resolution of symptoms occurred following the administration of the “vagolytic rescuer” this was a case of laryngospasm induced by vagal stimulation? We are inclined to think that i.v. fluids and ephedrine restored systemic blood pressure and cerebral perfusion. It is comforting to know that an ”adequately sedated and arousable” patient is aroused by breathing difficulties. Whether or not this is a case of laryngospasm caused by vagal stimulation is debatable, however it is definitely a reminder of the importance of proper hydration and the significance of refraining from overzealous use of sedatives. A.Boztepe G.B.Yıldırım İstanbul, Turkey E-mail: aboztepe@superonline.com Conflict of Interest:None declared |
|||
|
|
|||
|
Kandasamy Subramani, (Currently) Consultant Anaesthetist Weston General Hospital, Weston-Super-Mare, UK
Send letter to journal:
|
Editor, we thank Dr. Chincholkar for his interest in our case report(1). My sincere apologies for the delay in responding, which is due to my relocation. To answer the queries raised by Dr. Chincolkar(2), the level of block before the dressing was opened was T11 bilaterally to sharp pain. It may have been higher, but we did not test further as the level was satisfactory for the dressing removal. Only part of the outer layer of the dressing was removed. The inner layers were still in place, the patient's leg was supported at his calf and the wound was not handled at any point. Thus, the idea that removal of dressing was the cause of laryngospasm is unlikely. It took at least 3 minutes for the laryngospasm to break and not immediately after the surgeons stopped removing the dressings. The measures described in our case report namely fluid loading and atropine prevented any further development of a high parasympathetic tone and this in our opinion explains the further uneventful course of the anaesthetic. We employed sharp pain as a modality of testing as most clinicians would do. We do agree that a simple pin prick test may not equate to the complex mechanisms involved in perception of surgical pain, but this is the most common method of testing level of block for regional anaesthesia in most clinical settings. The temporal summation is blocked in subarachnoid blocks(3) and not so well in epidural blocks(4). We disagree on the comment that the onset of bilateral blocks in lateral position is slow. There are multiple factors governing the spread and onset of subarachnoid block(5). Dr. Chincholkar quotes a study of regional anaesthesia for caesarean section(6). The complex changes during pregnancy by no means would be comparable to our male patient undergoing foot surgery. Instead, I would draw his attention to a study(7), where the onset of bilateral sensory block to T10 with 15 mg of 0.5% bupivacaine with 8% glucose was a median of 2 with a range of 2-10 minutes. The dose is slightly higher than the 12.5 mg 0.5% bupivacaine with 8% glucose that we administered. In our patient, the block was performed in the right lateral position and the patient was turned supine immediately and hence it is unlikely that the block was unilateral. As Dr. Chincholkar describes our case report, it was rather perplexing to us too when we were confronted with laryngospasm during a spinal anaesthetic. What we did was to follow the “ABC” as we do in any emergency. As discussed in the case report, we were in the process of securing the airway with an endotracheal tube which was not possible without optimising the haemodynamic parameters. Haemodynamic optimization involved bolus of intravenous fluid, atropine and ephedrine. In our opinion, the laryngospasm responded to the above measures, which were mostly vagolytic. At the time of resuscitation, we did not have the least suspicion that what we saw could have been a manifestation of high parasympathetic tone secondary to relative hypovolemia! Reference: 1. Subramani K, Paul A. Laryngospasm during subarachnoid block. Br J Anaesth 2005; 94: 668-70. 2. Chincholkar MG. Laryngospasm during subarachnoid block. Br J Anaesth 2005; 95: 277. 3. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Zbinden AM. Spinal anaesthesia inhibits central temporal summation. Br J Anaesth 1997; 78: 88 -9. 4. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Fischer M, Zbinden AM. Temporal summation during extradural anaesthesia. Br J Anaesth 1995; 75: 634-5. 5. Hocking G, Wildsmith JA. Intrathecal drug spread. Br J Anaesth 2004; 93: 568-78. 6. Lewis NL, Ritchie EL, Downer JP, Nel MR. Left lateral vs. supine, wedged position for development of block after combined spinal-epidural anaesthesia for Caesarean section. Anaesthesia 2004; 59: 894-8. 7. Whiteside JB, Burke D, Wildsmith JAW. Comparison of ropivacaine 0.5% (in glucose 5%) with bupivacaine 0.5% (in glucose 8%) for spinal anaesthesia for elective surgery. Br J Anaesth. 2003; 90: 304-308. Subramani Conflict of Interest:None declared |
|||
|
|
|||
|
Mahindra G Chincholkar West Cumberland Hospital, Whitehaven, UK
Send letter to journal:
|
Editor-The case report by Subramani K and Paul A was quite perplexing. The authors proposed that the laryngospasm was secondary to an increased parasympathetic tone resulting from the subarachnoid blockade.1 There are a few points that the authors have not clarified. What was the method by which they tested the level of sensory blockade after injecting the drug in the subarachnoid space? Why did the patient recover rapidly after the stimulus (removal of dressing) was removed? How does an increased parasympathetic tone as a result of subarachnoid blockade explain the further uneventful course? It seems improbable that the laryngospasm responded to atropine and ephedrine. I would like to put forth a rather simplistic explanation for the laryngospasm- a mere response to pain experienced by the patient. An apparently ‘adequate’ (in extent) spinal may fail because the block has been tested using a stimulus of significantly different modality or intensity than the planned surgery.2 A simple single stimulus such as pinprick or cold may be blocked, but spinal cord mechanisms may result in repeated stimuli (temporal summation) or stimuli from adjacent regions (spatial summation), evoking pain.2 The subarachnoid block was performed in the right lateral position. The onset of bilateral block has been shown to be slower with blocks performed in the lateral position.3 The authors have not made it clear if the block till T11 was bilateral. All these factors alone or in combination, can explain why the patient had laryngospasm. E-mail: cmahindra@gmail.com 1. Subramani K, Paul A. Laryngospasm during subarachnoid block. Br J Anaesth 2005; 94:668-670 2. Hocking G, Wildsmith JAW. Intrathecal drug spread. Br J Anaesth 2004; 93: 568-578 3. Lewis NL, Ritchie EL, Downer JP, Nel MR. Left lateral vs. supine, wedged position for development of block after combined spinal-epidural anaesthesia for Caesarean section. Anaesthesia 2004; 59: 894-898 Conflict of Interest:None declared |
|||