Correspondence / American Journal of Emergency Medicine 38 (2020) 1679-1694 1683

E-mail address: [email protected].

Guy L. Weinberg

University of Illinois at Chicago College of Medicine, Jesse Brown Veterans

Administration Medical Center, Chicago, IL, USA

?Corresponding author.

E-mail address: [email protected].

27 February 2020

https://doi.org/10.1016/j.ajem.2020.03.065

References

1. Sidlak AM, Yanta JH, Lynch MJ. Intrathecal bupivacaine and morphine toxicity leading to transient hypotension and delayed status epilepticus. Am J Emerg Med 2020;38 (8):1683.
2. Lutfy K, Woodward RM, Keana JF, Weber E. Inhibition of clonic seizure-like excitatory effects induced by intrathecal morphine using two NMDA receptor antagonists: MK- 801 and ACEA-1011. Eur J Pharmacol 1994;252:261-6.
3. Yoburn BC, Lutfy K, Sierra V, Tortella FC. Tolerance develops to spinal morphine analgesia but not morphine-induced convulsions. Eur J Pharmacol 1990;176: 63-7.
4. Kronenberg MF, Laimer I, Rifici C, Saltuari L, Bramanti P, Moriggl U, et al. Epileptic sei- zure associated with intracerebroventricular and intrathecal morphine bolus. Pain 1998;75:383-7.
5. Sauter K, Kaufman HH, Bloomfield SM, Cline S, Banks D. Treatment of high-dose intra- thecal morphine overdose. Case report. J Neurosurg 1994;81:143-6.
6. Yilmaz A, Sogut A, Kilinc M, Sogut AG. Successful treatment of intrathecal morphine overdose. Neurol India 2003;51:410-1.
7. Fettiplace MR, Weinberg G. The mechanisms underlying Lipid resuscitation therapy. Reg Anesth Pain Med 2018;43:138-49.

   Intrathecal bupivacaine and morphine toxicity leading to transient hypotension and delayed status epilepticus

   We appreciate the thoughtful and constructive feedback sub- mitted. We certainly acknowledge the potential contribution of morphine to the clinical presentation of our patient [1-4], but the responsibility of any one drug to the presentation is largely un- knowable without data on the toxicity of intrathecal bupivacaine. Excessive CNS delivery of each drug could logically be anticipated to cause deleterious effects. It would be overly dismissive to ex- clude bupivacaine’s potential contribution. First, bupivacaine was administered in an overdose of equal proportion relative to its therapeutic spinal dose as morphine. Second, there are no prior re- ports of intrathecal bupivacaine administration at a similar dose as observed in our case. Additionally, direct neuronal toxicity from bupivacaine and/or other local anesthetics has previously been de- scribed [5]. Finally, though cases of intrathecal morphine toxicity are present in the literature, they are rare and limited by confound- ing factors with the dose of morphine in our case being lower than previous cases (100 mg vs 250-510 mg) [2-4]. In one case, a patient was found to have an intracranial hemorrhage [3]. In all three re- ports, high doses of naloxone were administered which two au- thors felt could have led to precipitated withdrawal contributing to the clinical picture [3,4]. Cessation of Naloxone therapy in the latter case led to resolution of Severe hypertension [4]. Thus, con- tinued or higher dosing of naloxone may not be warranted and po- tentially counterproductive. In fact, more aggressive therapies were performed in these case reports such as CSF irrigation and drainage, and intravenous barbiturate infusions [2-4]. In our case of severe toxicity, the response to therapy and relatively abbrevi- ated course may have indicated a potential benefit of intravenous fat emulsion (IFE). Ultimately, the “clinical pearls” that we drew from our experience are 1) Cardiotoxicity after an intrathecal bupivacaine overdose was limited, and 2) While antidotal thera- pies have been suggested in case reports following intrathecal

   drug delivery overdose, standard aggressive critical care of status epilepticus should not be delayed or subverted by reliance on those hypothesized, but largely unstudiED treatments.

   Alexander M. Sidlak, MD* Joseph H. Yanta, MD

   Division of Medical Toxicology, Department of Emergency Medicine, University of Pittsburgh School of Medicine, USA

   *Corresponding author at: Division of Medical Toxicology, Department of Emergency Medicine, University of Pittsburgh School of Medicine, USA.

   E-mail address: [email protected].

   Michael J. Lynch MD

   Pittsburgh Poison Center, Pittsburgh, PA, USA

   31 March 2020

   https://doi.org/10.1016/j.ajem.2020.03.064

   References

   Yoburn BC, Lufty K, Sierra V, Tortella FC. Tolerance develops to spinal morphine anal- gesia but not morphine-induced convulsions. Eur J Pharmacol 1990;176:63-7.

8. Ylimaz A, Sogut A, Kilinc M, Sogut AG. Succesful treatment of intrathecal morphine overdose. Neurol India 2003;51:410-1.
9. Sauter K, Kaufman HH, Bloomfield A, et al. Treatment of high-dose intrathecal mor- phine overdose: care report. J Neurosurg 1994;81(1):143-6.
10. Groudine SB, Cresanti-Daknis C, Lumb PD. Successful treatment of a massive intrathe- cal morphine overdose. Anesthesiology 1995;82(1):292-5.
11. Verlinde M, Hollmann MW, Stevens MF, et al. Local anesthetic-induced neurotoxicity. Int J Mol Sci 2016;17(2):339.

    Flow-safe disposable CPAP efficiency in cardiogenic pulmonary oedema

    To Editor,

    We have read with great interest the study “Is flow-safe disposable continuous positive airway pressure (CPAP) system as effective as non- invasive mechanical ventilation (NIMV) in the treatment of acute cardio- genic pulmonary oedema”, performed by Ilhan et al. and published on American Journal of Emergency Medicine [1], where two treatment op- tions in patients with cardiac pulmonary edema in an emergency depart- ment are compared. We congratulate the authors for this original contribution. The authors consider that both options have a solid basis of application in patients with cardiogenic pulmonary edema. However, we consider that there are some points to consider for an adequate eval- uation of the results:

    Flow-safe CPAP settings. We consider that the authors should pro- vide a more detailed description of flow-safe CPAP methodology, namely on titration.

12. Duration treatments: we consider that the authors base the use of slow-safe CPAP system in emergency department. However, the treatment time compared to the NIMV are not well clarified nor are the emergency department length stay in both groups.
13. Discrepancy on COPD prevalence: as the authors remarked in dis- cussion section, COPD prevalence was significantly higher on NIMV group. This is a factor of major concern regarding the efficacy of flow-safe CPAP, since COPD is a common comorbidity in acute car- diogenic pulmonary oedema, both conditions promoting each other aggravation. Also, there is a significant different on presence of initial hypercapnia, with NIMV being used preferably on hypercapnic patients.