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After my previous post, two days ago
#Case_03 Sux apnea sucks, but was it Sux?
We got a new case
90 kg male, with scheduled thyroid tumor resection. Operation lasts 3 hours (was performed by one of the elite surgeons in Iraq, very complicated with wide neck dissection, even the team was aware of any complication like brain edema and even Tracheostomy kit was standby}. The operation went well without using Tracheostomy, patient well sedated, at the end the patient starts to wake up, reversal of nmb done by administrating 2.5 mg neostigmine /1.2 Atropine. Once extubation done, the patient rapidly deteriorated, unable to breath and lock jaw happened (the later is my diagnosis)- beside tracheomalacia was differentialy diagnosed by them, his SPO2 went down to 20%, Surgeon was about to reexplore and put needle cricothyrodectomy, the Anesthesiologist and for emergency purpose gave 300 mg of Succinylcholine, the patient fully relaxed, SPO2 raised after good ventilation by Mask, and was able to tube the patient back, and the surgeon performed Tracheostomy successfully. Interestingly the patient restored spontaneous breathing after 10 minutes and once the surgery team finished Tracheostomy, patient was discharged from the OR.
So between the time of administering neostigmine/Atropine and later Succinylcholine was less than 15 minutes!
Previously in the other post, as we know there is a caution of not to administer succinylcholine after neostigmine (window time 1-2 hours)
How will you explain what happened in this case!
My explanation (If I am wrong correct me), the dose of neostigmine 2.5 mg wasn't enough to inhibit Acetylcholinestrase (partial reversal happened), as we know each Acetylcholinestrase can hydrolyze 25000 Ach molecules / seconds. This would explain the distribution of the neostigmine wasn't enough to act as AChE inhibitors [as we know the process is by oxydiaphoretic (or ‘acid-transferring’) inhibitors: act as an alternative substrate for AChE, producing a more stable carbamylated enzyme complex. Subsequent hydrolysis of the complex and thus reactivation of the enzyme is slow. - A to Z Anesthesia and Intensive care and perioperative medicine 5th edition]
So, when Succinylcholine administred, here the 300 mg, only 30 mg reached the synthetic cleft and the rest 270 mg being hydrolyzed by plasma chlinestrase aka Pseudocholinesterase. So, the remaining 30 mg was acting like competitive (its role is not competitive) at ACh-Nicotinic receptors with what left AChE who is hydrolyzing ACh. (did we induce phase II block? - this is a Benign question). So the time of dissociation of Succinylcholine from the receptor is about 10 minutes and that what happened and it was hardly and competitively replaced by ACh and although conformational changes happened, but Ach sought normal receptor first (Or both worked together, one is Succinylcholine acting on fatigue the muscles to get paralysis while Ach maintained regular exercise at the receptor - such a complexity)
So if this patient gained full recovery, in such window time, while the other patient in the previous post, the time was 3 hours and a half after the last neostigmine/atropine was given - did this will explain and address that the previous patient had scoline apnea or what? Taking into the consideration of the same dose of neostigmine 2.5 mg was given for both patients!
As first world Anesthesiologists, will you advise us to use the optimal dose of neostigmine (50 - 70 mcg/kg) not what I saw only 2.5 mg one ampoule and if something happened we can repeat the dose, but mostly 2.5 mg is enough as we have seen in our practice!
Thanks for reading, this is a scientific debate!
Amir
#Case_03 Sux apnea sucks, but was it Sux?
We got a new case
90 kg male, with scheduled thyroid tumor resection. Operation lasts 3 hours (was performed by one of the elite surgeons in Iraq, very complicated with wide neck dissection, even the team was aware of any complication like brain edema and even Tracheostomy kit was standby}. The operation went well without using Tracheostomy, patient well sedated, at the end the patient starts to wake up, reversal of nmb done by administrating 2.5 mg neostigmine /1.2 Atropine. Once extubation done, the patient rapidly deteriorated, unable to breath and lock jaw happened (the later is my diagnosis)- beside tracheomalacia was differentialy diagnosed by them, his SPO2 went down to 20%, Surgeon was about to reexplore and put needle cricothyrodectomy, the Anesthesiologist and for emergency purpose gave 300 mg of Succinylcholine, the patient fully relaxed, SPO2 raised after good ventilation by Mask, and was able to tube the patient back, and the surgeon performed Tracheostomy successfully. Interestingly the patient restored spontaneous breathing after 10 minutes and once the surgery team finished Tracheostomy, patient was discharged from the OR.
So between the time of administering neostigmine/Atropine and later Succinylcholine was less than 15 minutes!
Previously in the other post, as we know there is a caution of not to administer succinylcholine after neostigmine (window time 1-2 hours)
How will you explain what happened in this case!
My explanation (If I am wrong correct me), the dose of neostigmine 2.5 mg wasn't enough to inhibit Acetylcholinestrase (partial reversal happened), as we know each Acetylcholinestrase can hydrolyze 25000 Ach molecules / seconds. This would explain the distribution of the neostigmine wasn't enough to act as AChE inhibitors [as we know the process is by oxydiaphoretic (or ‘acid-transferring’) inhibitors: act as an alternative substrate for AChE, producing a more stable carbamylated enzyme complex. Subsequent hydrolysis of the complex and thus reactivation of the enzyme is slow. - A to Z Anesthesia and Intensive care and perioperative medicine 5th edition]
So, when Succinylcholine administred, here the 300 mg, only 30 mg reached the synthetic cleft and the rest 270 mg being hydrolyzed by plasma chlinestrase aka Pseudocholinesterase. So, the remaining 30 mg was acting like competitive (its role is not competitive) at ACh-Nicotinic receptors with what left AChE who is hydrolyzing ACh. (did we induce phase II block? - this is a Benign question). So the time of dissociation of Succinylcholine from the receptor is about 10 minutes and that what happened and it was hardly and competitively replaced by ACh and although conformational changes happened, but Ach sought normal receptor first (Or both worked together, one is Succinylcholine acting on fatigue the muscles to get paralysis while Ach maintained regular exercise at the receptor - such a complexity)
So if this patient gained full recovery, in such window time, while the other patient in the previous post, the time was 3 hours and a half after the last neostigmine/atropine was given - did this will explain and address that the previous patient had scoline apnea or what? Taking into the consideration of the same dose of neostigmine 2.5 mg was given for both patients!
As first world Anesthesiologists, will you advise us to use the optimal dose of neostigmine (50 - 70 mcg/kg) not what I saw only 2.5 mg one ampoule and if something happened we can repeat the dose, but mostly 2.5 mg is enough as we have seen in our practice!
Thanks for reading, this is a scientific debate!
Amir