References

Correspondence / American Journal of Emergency Medicine 31 (2013) 873-885

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Narat Srivali MD Supawat Ratanapo MD

Menzin J, White LA, Friedman M, et al. Factors associated with failure to correct the international normalized ration following fresh frozen plasma administration among patients treated for warfarin-related major bleeding. Thromb Haemost 2012;107:662-72.

Wiedermann CJ, Stockner I. Warfarin-induced Bleeding complications - clinical presentation and therapeutic options. Thromb Res 2008;122 Suppl 2:S13-8: S13-8.

Singer DE, Albers GW, Dalen JE, et al. antithrombotic therapy in atrial fibrillation: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008;133:546S-92S.

O’Shaughnessy DF, Atterbury C, Bolton MP, et al. Guidelines for the use of fresh- frozen plasma, cryoprecipitate and cryosupernatant. Br J Haematol 2004;126: 11-28.

Brody DL, Aiyagari V, Shackleford AM, et al. Use of recombinant factor VIIa in patients with warfarin-associated intracranial hemorrhage. Neurocrit Care 2005;2: 263-7.

Hyperkalemia-induced pacemaker dysfunction?

To the Editor,

We read with great interest the article by Muck et al [1]. The authors reported a very interesting case surviving extreme hyperka- lemia. We also recently had a case of hyperkalemia-induced pace- maker dysfunction manifested as failure of pacemaker capture and leading to unnecessary invasive pacemaker evaluation.

An 86-year-old man with ischemic cardiomyopathy status post-Implantable cardioverter-defibrillator implantation and com- plete atrioventricular block requiring permanent pacemaker with the rate-responsive accelerometer-based (DDDR) mode admitted for implantation of a left ventricular lead for cardiac resynchro- nization therapy. After the procedure, the patient subsequently developed failure to capture of the pacemaker stimulus with a wide idioventricular rhythm on 12-lead Electrocardiography (Fig. 1).

He was asymptomatic with a normal blood pressure. However, because of the concern that the prior procedure might have inter- fered with his Pacemaker function, he was brought down to electro- physiology laboratory and the pacemaker pocket was re-explored. No problems with the pacemaker generator or pacemaker wire were identified. The patient was later found to have hyperkalemia with a potassium level of 7.1 mEq/dL. He was treated with Calcium gluconate, insulin with dextrose, and Kayexalate, and the potassium level decreased to 4.6 mEq/dL in 3 hours. His cardiac rhythm re- turned to a normal ventricular paced rhythm with full capture (Fig. 2). He remained hemodynamically stable and was discharged the following day.

Pacemaker dysfunction is usually due to mechanical problems such as lead fracture, lead dislodgement, or generator malfunction. However, hyperkalemia is an uncommon but easily correctable cause of pacemaker dysfunction, which can manifest as failure to capture [1,2], as in our patient. Hyperkalemia causes a decrease in myocardial excitability, which eventually leads to a decreased response to pace- maker stimulus [3,4]. It is important to think about hyperkalemia before considering an invasive procedure to evaluate for technical or primary pacemaker dysfunction. Failure to recognize this can lead to a Delay in diagnosis, unnecessary invasive procedures, and poten- tially fatal hemodynamic deterioration.

? Authors’ contributions: All authors had access to the data and a role in writing the manuscript.

Wisit Cheungpasitporn MD Daych Chongnarungsin MD Edward F. Bischof MD

Department of Medicine, Bassett Medical Center

Cooperstown, NY 13326, USA E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2013.01.021

References

1. Muck PM, Letterer S, Lindner U, Lehnert H, Haas CS. Beating the odds-surviving extreme hyperkalemia. Am J Emerg Med 2012;30(1):250.e1-4.
2. Schiraldi F, Guiotto G, Paladino F. Hyperkalemia induced failure of pacemaker capture and sensing. Resuscitation 2008;79(1):161-4.
3. Kahloon MU, Aslam AK, Aslam AF, Wilbur SL. Hyperkalemia induced failure of atrial and ventricular pacemaker capture. Int J Cardiol 2005;105(2): 224-6.
4. Sestito A, Lanza GA, Montebelli MR, Zecchi P. Images in cardiovascular medicine. Pacemaker failure caused by hyperkalemia. Ital Heart J 2002;3(2): 141-2.

   Reply to: Brain computed tomographic scan findings in Acute opium overdose patients

   To the Editor,

   I read with great interest a recent article published by Farkhondeh Jamshidi et al-“Brain computed tomographic scan findings in acute opium overdose patients” in the recent issue of American Journal of Emergency Medicine (Volume 31, issue 1, January 2013, Pages 50-53) [1].

   As a practicing neurointensivist, I found this article very relevant to my practice as I often encounter such cases. The authors have tried to correlate the opium poisoning/overdose with computed tomographic (CT) scan changes. However, one is forced to stop and wonder about 2 vital questions.

   The authors mention that “no other drug overdose in this study as per patient’s history.” This is a crucial question as polysubstance abuse is rule than exception. Furthermore, other substances of abuse could have varied effects on the central nervous system with potential changes in CT scan. I wonder if authors had the data for toxicology screens. Without these data, the conclusions are shaky, as the history may not be accurate in such population. Next, authors mention that “subjects with history of CNS disorders were excluded.” However, authors have not elaborated what criteria were used to exclude “Central Nervous system disorders,” as any preexisting illness would change the interpretation drasti- cally. Did authors have previous CT scan results to corroborate? Without these answers, I would be hesitant to apply these results in clinical practice.

   Sankalp Gokhale, MD Department of Neurology (Neurocritical care and stroke) Duke University Hospital, Durham, NC, USA, 27710

   E-mail address: [email protected]

   http://dx.doi.org/10.1016/j.ajem.2013.01.026

   880 Correspondence / American Journal of Emergency Medicine 31 (2013) 873-885

   

   Fig. 1. ECG revealed failure to capture of the pacemaker stimulus with a wide idioventricular rhythm on 12-lead ECG.

   

   Fig. 2. ECG revealed a normal ventricular paced rhythm with full capture.

   Reference

   [1] Babak Sadighi FJ, Aghakhani K, Sanaei-Zadeh H, Emamhadi M, Zamani N. Brain computed tomographic scan findings in acute opium overdose patients. (AJEM, Jan 2013, 50-53)

   How can we diagnose pure opium overdose cases in retrospective medical chart reviews?

   To the Editor,

   We are grateful for the interest in our article “Brain computed tomographic scan findings in acute opium overdose patients” [1]. In retrospective studies, such as ours, some limitations are inevitable. For instance, exclusion of the multidrug exposures based on the history is one of them that has been mentioned as the most important limitation of our study in the “Discussion.” Regarding the use of toxicology screening for exclusion of other substances of abuse, it should be mentioned that each drug of abuse screening test may exhibit a different cross-reactivity profile. Depending on this profile, drug abusers may have false-positive or false-negative results [2,3]. Furthermore, in drug screens, some substances of abuse cross-react with other medications [3,4]. Therefore, with these limitations, the results of such Screening tests may sometimes create confusion except

   for when they are confirmed by retesting using a nonimmunologic test [3,5]. In addition, the major problem with opiates is that several opiates are metabolized into each other. For example, morphine is a metabolite of codeine and heroin as well as a constituent of opium. So, heroin exposure cannot be distinguished from opium exposures using such screening tests. In addition, Synthetic opioids are often not detected by these tests. With respect to the aforementioned points, even if few patients’ samples were sent to perform toxicology screening tests and reports of their results were available in the files, these results would not be valuable for the inclusion or exclusion of the cases. However, attention to the following points shows that our results and conclusion are reliable: (1) Opium overdose is very common in our country [6-9]. (2) In addition to the history, diagnosis of the isolated opium overdose cases in medical charts has been made based on clinical manifestations that are different from overdose with other non-Opioid abused drugs. (3) Cocaine and crack cocaine abuse is rare in Iran. (4) Although acute overdose by amphetamines, methamphetamines, and ecstasy is not so uncommon in our country [9], of the most common-if any-findings of their overdose similar to that of cocaine are subarachnoid or intracerebral hemorrhages, which were not detected in none of our cases [10]. (5) Cannabis is one of the most commonly abused drugs in our community [9]. However, the relation of ischemic strokes with its overdose has not yet been established [10]. (6) In addition to other exclusion criteria that have been mentioned in our article, some cases of previously diagnosed structural changes on brain computed tomographic scan were also found that were not included. These