American Journal of Emergency Medicine 33 (2015) 1831–1839
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Correspondence Mustafa Tanrıseven, MD Department of General Surgery, Diyarbakır Military Hospital Diyarbakır, Turkey
An approach to markedly elevated blood pressure in hypertensive patients without acute organ damage ☆
http://dx.doi.org/10.1016/j.ajem.2015.06.050 To the Editor, We read the article “Blood pressure treatment and outcomes in hypertensive patients without acute organ damage: a retrospective cohort” written by Levy et al [1] with great interest. They concluded that there was no evidence of benefit with treatment to acutely lower blood pressure in the patients with markedly elevated blood pressure and absent signs or symptoms of acute target organ damage [1]. Lowering blood pressure quickly has no proven benefit in patients without acute organ damage [2]. In contrast, there are studies showing the related complications of reducing blood pressure suddenly in this kind of patients [2]. The potential danger of acutely decreasing blood pressure is the risk of autoregulatory disorder of cerebral and renal perfusion that leads to cerebral and renal injury [3]. We have to treat patients, not numbers, but does that not mean we should be treating symptomatic patients as well as not overtreating asymptomatic patients? Are we realistic to conclude that symptomatic patients—albeit without end-organ damage—should not be treated in the emergency department (ED)? Blood pressure can be reduced slowly in patients who have headache, severe anxiety, respiratory distress, or epistaxis, by following them up for a few hours in the ED [4]. Start with the principle “do not harm the patient” and determining which patients can be discharged without treatment: the patients who are suitable for primary care, whose precipitating factors are eliminated, who will eager to continue with the previous effective medication, and who can return within 24 hours for control examination. The most logical approach is to prescribe the oral medication in the ED that the patient had already been on or discontinued. A consensus needs to be developed on the management of patients with markedly elevated blood pressure and lack of clinical evidence of acute target organ damage in the ED. Hakan Sarlak, MD Department of Internal Medicine, Diyarbakır Military Hospital Diyarbakır, Turkey Corresponding author. Department of Internal Medicine Diyarbakır Military Hospital, Seref Inaloz St. 21100 Yenisehir Diyarbakır, Turkey Tel.: +90 412 2288225; fax: +90 412 2236732 E-mail address:
[email protected] Salim Ozenc, MD Department of Family Medicine, Diyarbakır Military Hospital Diyarbakır, Turkey Ibrahim Arzıman, MD Department of Emergency Medicine, Gulhane Military Medical Faculty Ankara, Turkey ☆ There is no conflict of interests. 0735-6757/© 2015 Elsevier Inc. All rights reserved.
References [1] Levy PD, Mahn JJ, Miller J, Shelby A, Brody A, Davidson R, et al. Blood pressure treatment and outcomes in hypertensive patients without acute organ damage: a retrospective cohort. Am J Emerg Med 2015. http://dx.doi.org/10.1016/j.ajem.2015.05.036. [2] Yanturali S, Akay S, Ayrik C, Cevik AA. Adverse events associated with aggressive treatment of increased blood pressure. Int J Clin Pract 2004;58(5):517–9. [3] Varon J, Marik P. Clinical review: the management of hypertensive crises. Crit Care 2003;7:374–84. [4] Adhikari S, Mathiasen R. Epidemiology of elevated blood pressure in the ED. Am J Emerg Med 2014;32(11):1370–2.
Response to “An approach to markedly elevated blood pressure in hypertensive patients without acute organ damage” Thank you for your interest in our article. We are in agreement with you that a cautious approach to blood pressure reduction in hypertensive patients without acute organ damage is warranted and acknowledge that this has been emphasized in several other publications. However, many emergency physicians still retain a level of discomfort withholding antihypertensive therapy for patients who have markedly elevated blood pressure and the purpose of our study was to show that outcomes are equivocal with such an approach. In doing so, we provide evidence to support the decision not to treat numbers alone. When symptoms potentially attributable to acute organ damage are present, further diagnostic workup and treatment directed at the causal factors, including antihypertensive therapy, may be indeed be necessary. That said, there is no direct benefit associated with blood pressure reduction for conditions such as anxiety or headache, and instead treatment with anxiolytic or pain medication is more likely to achieve desired therapeutic effects. We agree that for patients who have persistent blood pressure elevation posttreatment of such symptoms, initiation, reinitiation, or titration of oral antihypertensive therapy coupled with outpatient follow-up (though not necessarily within 24 hours) is warranted. As we have recently shown [1], emergency physicians can safely and efficaciously prescribe oral medication for management of hypertension and broader appreciation of this, perhaps through development of a consensus statement would be beneficial. Phillip D. Levy, MD, MPH* Robert D. Welch, MD, MS Department of Emergency Medicine, Wayne State University Detroit, MI ⁎Corresponding author. E-mail address:
[email protected] http://dx.doi.org/10.1016/j.ajem.2015.06.051
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Reference [1] Brody A, Rahman T, Reed B, Millis S, Ference B, Flack JM, et al. Safety and efficacy of antihypertensive prescription at emergency department discharge. Acad Emerg Med 2015;22:632–5.
Neuroleptic malignant syndrome and reversible magnetic resonance imaging changes: a new insight☆,☆☆ To the Editor, Jain et al [1] have reported reversible brain magnetic resonance imaging (MRI) changes in neuroleptic malignant syndrome (NMS). Previous reports revealed similar such changes in different parts of cerebrum and cerebellum [1,2]. Apart from mechanisms suggested by the authors [1], we would like to mention additional mechanisms for NMS such as those related to electrolyte “sodium” and another to chemical “glutamate” and the diagnostic role of functional MRI [3]. Jain et al [1] have noted hypernatremia, and the association between hypernatremia and NMS has been demonstrated earlier. Hypernatremia also causes reversible splenial lesion [4], as glutamate has excitotoxicity [5] and has been implicated in NMS. Moreover, increased intracranial level of glutamate in NMS is responsible for symptoms such as hyperthermia, tremor, and dystonia and MRI changes [5]. Functional MRI (H-proton magnetic resonance spectroscopy [HMRS]) used to assess the concentration of neurotransmitter is progressing. Chatterjee [5] used a single-voxel HMRS to verify the excess of glutamate concentration in NMS, which was followed by multivoxel imaging to map the concentration of glutamate. Thus, HMRS is useful to diagnose NMS and to assess the severity [5,6]. However, further studies are warranted to confirm or refute the observations as well as to explore any other mechanisms for NMS so as introduce appropriate therapeutic measures. Shah Sweni, MD Department of Emergency and Critical Care Erode Emergency Care Hospital, Erode, Tamil Nadu, India Department of Internal Medicine, Chennai Medical College Hospital and Research Center, Irungalur, Trichy, Tamil Nadu, India Subramanian Senthilkumaran, MD Department of Emergency and Critical Care Erode Emergency Care Hospital, Erode, Tamil Nadu, India Corresponding author. Department of Emergency & Critical Care Medicine, Erode Emergency Care Hospital Erode, Tamil Nadu, India Tel.: +91 9846349444, +91 9994634444 (Mobile) E-mail address:
[email protected] Namasivayam Balamurugan, MD, DM Department of Neurosciences, SIMS Chellam Hospital Salem, Tamil Nadu, India Ponniah Thirumalaikolundusubramanian, MD Department of Internal Medicine, Chennai Medical College Hospital and Research Center, Irungalur, Trichy, Tamil Nadu, India http://dx.doi.org/10.1016/j.ajem.2015.07.003 References [1] Jain RS, Gupta PK, Gupta ID, Agrawal R, Kumar S, Tejwani S. Reversible magnetic resonance imaging changes in a case of neuroleptic malignant syndrome. Am J Emerg Med 2015;33(8):1113.e1–3 [PubMed PMID: 25769796]. ☆ Financial support—nil. ☆☆ Conflict of interest—nil.
[2] Al-Edrus S, Norzaini R, Chua R, Puvanarajah S, Shuguna M, Muda S. Reversible splenial lesion syndrome in neuroleptic malignant syndrome. Biomed Imaging Interv J 2009; 5(4):e24 [PubMed PMID: 21610992. Pubmed Central PMCID: 3097717]. [3] Arnaout MS, Antun FP, Ashkar K. Neuroleptic malignant syndrome with olanzapine associated with severe hypernatremia. Hum Psychopharmacol 2001;16(3):279–81 [PubMed PMID: 12404581]. [4] Maeda M, Tsukahara H, Terada H, Nakaji S, Nakamura H, Oba H, et al. Reversible splenial lesion with restricted diffusion in a wide spectrum of diseases and conditions. J Neuroradiol 2006;33(4):229–36 [PubMed PMID: 17041527]. [5] Chatterjee A. Glutamate-based magnetic resonance spectroscopy in neuroleptic malignant syndrome. Ann Indian Acad Neurol 2014;17(1):123–4 [PubMed PMID: 24753679. Pubmed Central PMCID: 3992752]. [6] Coutanche MN, Thompson-Schill SL, Schultz RT. Multi-voxel pattern analysis of fMRI data predicts clinical symptom severity. NeuroImage 2011;57(1):113–23 [PubMed PMID: 21513803. Pubmed Central PMCID: 3105443].
How do emergency medicine residency core faculty obtain their ultrasound training for credentialing?
To the Editor, The evolution of emergency ultrasound (EUS) in resident education began in the early 1990s with the American College of Emergency Physicians (ACEP) publishing their first position statement supporting the use of ultrasound (US) by trained physicians [1]. Soon afterwards, The Society for Academic Emergency Medicine (SAEM) endorsed this statement and recommended formal EUS training for all emergency residency programs [2]. In 1994, Mateer et al published the “Model curriculum for physician training in emergency ultrasonography” that laid the template for standardized EUS education [3]. In 1999, the American Medical Association passed resolution 802 and policy H-230.960, which recognized US being “within the scope of practice of appropriately trained physicians” and instructed each subspecialty to form their individual training requirements [4]. In 2001, the Model of the Clinical Practice of Emergency Medicine was published by the Accreditation Council for Graduate Medical Education that mandated residents become competent in EUS by the conclusion of training [5]. In 2007, the Council of Emergency Medicine Residency Directors (CORD) met with leaders in the field of emergency medicine (EM) to model US curriculum for residency training programs during the annual meeting of the SAEM. Members of CORD, SAEM, and ACEP attended a consensus conference in New Orleans the following year to formalize a curriculum that was called the CORD EUCC. Their recommendations were that residency programs train their residents in the evaluation of the trauma patient, imaging in pregnancy, aortic imaging, emergent cardiac imaging, biliary imaging, renal imaging, evaluation of deep venous thrombosis, thoracic imaging, soft tissue and musculoskeletal imaging, and procedural imaging. It was recommended that all EM residency programs have a full-time faculty member assume the role of US Director and that a minimum of 50% of core faculty be designated as “US faculty.” These individuals would have to be credentialed in EUS by the host institution [6]. Later that year, CORD proposed a formal EUS curriculum for EM program directors, entitled the “Resident Training in Emergency Ultrasound: Consensus Recommendations from the 2008 Council of Emergency Medicine Residency Directors Conference” [7]. Building on this in 2012, the Accreditation Council for Graduate Medical Education designated EUS as one of the patient care subcompetencies (PC12) of the 24 milestone competencies for EM residency graduates [8]. The focus of this study was to evaluate how core faculty became credentialed in EUS. Based on the Emergency Ultrasound Guidelines, there are 2 pathways to obtain EUS credentialing. The first is the residency-based pathway, in which faculty has had formal EUS training during residency. The second is the practice-based pathway for physicians who did not receive US training during residency.