- Email: [email protected]
Right ventricular diastolic function in patients with community-acquired pneumonia
Correspondence / American Journal of Emergency Medicine 33 (2015) 1515–1535
cardiac output monitoring did not improve the primary end point of 28day mortality. In septic shock, mortality is high because of the complexity of the pathophysiology [2]. No particular monitoring system, but rather rapid global management, is likely to improve survival in these cases. More generally, in septic shock, hemodynamic studies aiming to reduce mortality often prove negative. Optimizing cardiac output does not improve mortality [3]; nor does a mean arterial pressure threshold of 80 to 85 mm Hg rather than 65 to 70 mm Hg [4], or introducing dopamine or norepinephrine [5]. Hemodynamic failure, which is one of the components of septic shock, is complex. Vasoplegia is the main element, but the underlying mechanism is poorly understood [6]. There is vascular hyporesponsiveness to amines [6]. There is left ventricle systolic deficit, defined as left ventricular ejection fraction less than 45%, in almost 60% of cases in the acute phase of septic shock [7]. Patients moreover show impaired microcirculation, with a reduced proportion of perfused microvessels and increased heterogeneity [8]. Microcirculation data in fact provide stronger prognostic evidence than global hemodynamic parameters such as blood pressure or heart rate [9]. Global systemic hemodynamic failure, however, does not seem to correlate with microcirculatory impairment [10], and is poorly understood and is just one of the factors involved in the severity and fatality associated with septic shock. It thus seems unlikely that benefit in terms of mortality can be provided by cardiac output monitoring or the macrocirculation data of the pulse-indicated continuous cardiac output monitor. Use of bundles is recommended by the Surviving Sepsis Campaign 2012 [11]: this is what improves mortality [12]. Recent studies have indeed shown that implementing an Early Goal-Directed Therapy protocol does not reduce mortality in septic shock as compared with usual care [13,14]. However, since the work of Rivers et al [15] in 2001 and the first guidelines of the Surviving Sepsis Campaign in 2004, management has enormously progressed. Our practice has indeed been greatly influenced by these guidelines, which probably in themselves represent the current standard of care. It is recommended to monitor cardiac output in certain types of shock, for diagnostic purposes and to follow the progress of treatment, particularly for inotropes [16]. In our opinion, in case of sepsis, arterial pulse contour analysis and transpulmonary thermodilution should at present be reserved to refractory septic shock. Seeking to improve survival in septic shock by monitoring one component of hemodynamic failure seems impractical. Criteria such as mechanical ventilation time or duration of intensive care seem better adapted. N. Mottard, MD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet, 69495 Pierre Bénite, France Corresponding author E-mail address: [email protected] B. Allaouchiche, PhD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet, 69495 Pierre Bénite, France EA 4174 Sepsis Inflammation Hémostase, Vetagro Sup-Campus Vétérinaire de Lyon, 1 Avenue Bourgelat, 69280 Marcy-l'Étoile, France A. Friggeri, MD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet, 69495 Pierre Bénite, France J. Bohé, PhD V. Piriou, PhD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet 69495 Pierre Bénite, France Université Claude-Bernard, Lyon 1, France
http://dx.doi.org/10.1016/j.ajem.2015.07.034
1521
References [1] Zhang Z, Ni H, Qian Z. Effectiveness of treatment based on PiCCO parameters in critically ill patients with septic shock and/or acute respiratory distress syndrome: a randomized controlled trial. Intensive Care Med 2015;41(3):444–51. [2] Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med 2013;369(9): 840–51. [3] Gattinoni L, Brazzi L, Pelosi P, Latini R, Tognoni G, Pesenti A, et al. A trial of goaloriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group. N Engl J Med 1995;333(16):1025–32. [4] Asfar P, Meziani F, Hamel J-F, Grelon F, Megarbane B, Anguel N, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014;370(17): 1583–93. [5] De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362(9):779–89. [6] Levy B, Collin S, Sennoun N, Ducrocq N, Kimmoun A, Asfar P, et al. Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside. Intensive Care Med 2010;36(12):2019–29. [7] Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock. Crit Care Med 2008;36(6): 1701–6. [8] De Backer D, Creteur J, Preiser J-C, Dubois M-J, Vincent J-L. Microvascular blood flow is altered in patients with sepsis. Am J Respir Crit Care Med 2002;166(1):98–104. [9] Ince C. The microcirculation is the motor of sepsis. Crit Care Lond Engl 2005;9(Suppl. 4): S13–9. [10] De Backer D, Creteur J, Dubois M-J, Sakr Y, Koch M, Verdant C, et al. The effects of dobutamine on microcirculatory alterations in patients with septic shock are independent of its systemic effects. Crit Care Med 2006;34(2):403–8. [11] Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med 2013;39(2):165–228. [12] Levy MM, Dellinger RP, Townsend SR, Linde-Zwirble WT, Marshall JC, Bion J, et al. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Intensive Care Med 2010; 36(2):222–31. [13] Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA, Pike F, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med 2014;370(18): 1683–93. [14] Peake SL, Delaney A, Bailey M, Bellomo R, Cameron PA, Cooper DJ, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med 2014;371(16): 1496–506. [15] Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, et al. Early goaldirected therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345(19):1368–77. [16] Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med 2014;40(12):1795–815.
Right ventricular diastolic function in patients with community-acquired pneumonia☆ To the Editor, We read with great interest the article “Is there a potential role for echocardiography in adult patients with community-acquired pneumonia? A pilot study” written by Yildirim et al [1]. They aimed to investigate left and right ventricular (RV) functions and aortic elastic properties and observe relationships between echocardiographic findings and inflammatory and cardiac serum biomarkers in communityacquired pneumonia (CAP) patients. They showed that CAP is associated with reduced levels of tricuspid annular plane systolic excursion and impaired elasticity of the ascending aorta, and these markers are correlated with the severity of the disease. We believe that these findings will act as a guide for further studies regarding echocardiographic evaluation of left and RV functions in patients with CAP. Tricuspid annular plane systolic excursion can be used routinely as a simple method of estimating RV systolic function but not diastolic function. Contrary to common belief, the right ventricle is not a passive chamber. Multiple studies have demonstrated that RV diastolic dysfunction usually occurs before apparent RV systolic dysfunction and RV dilatation. Therefore, it serves as an early and more easily quantifiable marker of subclinical RV dysfunction. A large number of acute and chronic diseases have been associated with RV diastolic dysfunction, including both pressure and volume ☆ There is no conflict of interest.
1522
Correspondence / American Journal of Emergency Medicine 33 (2015) 1515–1535
overload pathologies such as primary lung disease, congenital heart disease, cardiomyopathies, ischemic heart disease, and systemic diseases [2,3]. Right ventricular diastolic function has been evaluated using Doppler velocities of the transtricuspid flow (E, A, and E/A), tissue Doppler velocities of the tricuspid annulus (E′, A′, E′/A′), deceleration time, and isovolumic relaxation time. Most commonly used in recent studies are the tricuspid E/E′ ratio, right atrial (RA) area or volume, and diastolic strain rate. It has been shown to be a good correlation between the tricuspid E/E′ ratio and RA volume, and hemodynamic parameters. An E/E′ ratio if 4 or higher had high sensitivity and specificity for predicting RA pressure of 10 mm Hg or greater in noncardiac surgery intensive care unit patients [4]. The current study did not evaluate RV diastolic function and RA volume [1]. On the other hand, it would be better if they also evaluated RV function using other parameters including RV index of myocardial performance, myocardial acceleration during isovolumic contraction, and RV fractional area change. Because these quantitative measurement are simple and reproducible, they do not require sophisticated equipment or prolonged image analysis. We think that it might be helpful if the RV systolic and diastolic functions were assessed by using these quantitative parameters in patients with CAP in the further studies. Sait Demirkol, MD* Cengiz Ozturk, MD Sevket Balta, MD Murat Unlu, MD Zekeriya Arslan, MD Gulhane Military Medical Academy, School of Medicine Department of Cardiology, Ankara, Turkey ⁎Corresponding author at: Department of Cardiology Gulhane School of Medicine, Tevfik Saglam St, 06018 Etlik, Ankara, Turkey Tel.: +90 312 3044281; fax: +90 312 3044250 E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.07.022 References [1] Yıldırım B, Biteker FS, Basaran O, Alatas OD, Acar E, Sozen H, et al. Is there a potential role for echocardiography in adult patients with community-acquired pneumonia? A pilot study. Am J Emerg Med 2015. http://dx.doi.org/10.1016/j.ajem.2015.06.036 [Epub ahead of print]. [2] Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 2010;23:685–713. [3] Cardoso SM, Miyague NI. Right ventricular diastolic dysfunction in the postoperative period of tetralogy of Fallot. Arq Bras Cardiol 2003;80(2):198–201 [194–7]. [4] Sade LE, Gulmez O, Eroglu S, Sezgin A, Muderrisoglu H. Noninvasive estimation of right ventricular filling pressure by ratio of early tricuspid inflow to annular diastolic velocity in patients with and without recent cardiac surgery. J Am Soc Echocardiogr 2007;20:982–8.
No correlation between body size and hydromorphone analgesia in obese patients in ED
To the Editor, Obesity is associated with pain, and pain is the most common presentation in the emergency department [1,2]. The mainstay treatment
of moderate and severe pain in the emergency department is intravenous opioids, but the appropriate opioid dosing for obese patients is still in question. Due to their increased body sizes and altered fat-lean mass ratios, body size measures, such as lean body weight and ideal body weight, have been recommended and used to dose intravenous opioids in obese patients [3,4]. However, previous studies have neither confirmed nor disproved these dosing recommendations. The current study was a secondary analysis of a previously conducted prospective clinical trial in the emergency department at an academic urban hospital [5]. The study was approved by the institutional review board and registered with ClinicalTrials.gov (Identifier NCT01675778). Inclusion and exclusion criteria, as well as the study protocol, have previously been described [5]. Briefly, all study participants received 1 mg intravenous hydromorphone. Pain intensities (Numeric Rating Scale, or NRS) were collected before and 30 minutes after hydromorphone administration. Patient demographics, pain duration, location, and mechanism (injury vs noninjury) were recorded. When patients were more comfortable after the treatment, their weight (kilogram) and height (centimeter) were measured (Scale-Tronix; Scale-Tronix Inc, Carol Stream, IL). Various body size measures were calculated [6]. Scatterplots were constructed to show the relationships between different body size measures and clinical NRS changes 30 minutes after hydromorphone administration. Pearson correlation coefficients were also calculated. Statistical software STATA version 12.1 (Stata Corporation, College Station, TX) was used for data analysis. We had 73 study participants with body mass index (BMI) of 30 kg/m2 or greater. Their baseline characteristics are listed in Table. As shown in Figure, there were no statistically significant correlations between pain NRS changes and any of the body size measures examined here. The lack of the correlation between these body size measures and response to opioid analgesia may be explained by studies of opioid pharmacodynamics, which have failed to demonstrate an association between opioid plasma concentration and clinical analgesic effects [7]. Our study results do not support the recommendation to adjust hydromorphone doses based on any of the body size measures examined here. An initial fixed dose of intravenous hydromorphone should be used in obese patients with acute pain in the emergency department. Limitations to the current study included small sample size, short assessment time (30 minutes after hydromorphone administration), heterogeneous pain causes, bivariate association analysis without considering other influencing factors (sex, race, psychological, and genetic factors could also affect pain treatment response), and single-center study. In summary, the current analysis does not support adjusting opioid doses based on various body size measures in obese patients. An initial fixed dose of opioids should be used in obese patients with acute pain in the emergency department.
Shujun Xia, MD, PhD* Edward Chew, MD Dong Choe, MD Lenin Hernandez, BA Adrienne Birnbaum, MD, MS Department of Emergency Medicine, Jacobi Medical Center Albert Einstein College of Medicine, Bronx, NY *Corresponding author. Department of Emergency Medicine, Jacobi Medical Center, 1400 Pelham Parkway South, Bronx, NY 10461
Body size measures
Male
Female
BMI Ideal body weight (IBW) Lean body weight Body surface area Adjusted body weight Predicted normal weight
kg/m2 = TBW/height2 kg = 45.4 + 0.89 × [height (cm) − 152.4] + 4.5 kg = 9270 × TBW/(6680 + 216 × BMI) m2 = √[(height(cm) × TBW)/3600] kg = IBW + 0.4 × (TBW − IBW) kg = 1.57 × TBW − 0.0183 × BMI × TBW − 10.5
Same as male kg = 45.4 + 0.89 × [height (cm) − 152.4] kg = 9270 × TBW/(8780 + 244 × BMI) Same as male Same as male kg = 1.75 × TBW − 0.0242 × BMI × TBW − 12.6
cardiac output monitoring did not improve the primary end point of 28day mortality. In septic shock, mortality is high because of the complexity of the pathophysiology [2]. No particular monitoring system, but rather rapid global management, is likely to improve survival in these cases. More generally, in septic shock, hemodynamic studies aiming to reduce mortality often prove negative. Optimizing cardiac output does not improve mortality [3]; nor does a mean arterial pressure threshold of 80 to 85 mm Hg rather than 65 to 70 mm Hg [4], or introducing dopamine or norepinephrine [5]. Hemodynamic failure, which is one of the components of septic shock, is complex. Vasoplegia is the main element, but the underlying mechanism is poorly understood [6]. There is vascular hyporesponsiveness to amines [6]. There is left ventricle systolic deficit, defined as left ventricular ejection fraction less than 45%, in almost 60% of cases in the acute phase of septic shock [7]. Patients moreover show impaired microcirculation, with a reduced proportion of perfused microvessels and increased heterogeneity [8]. Microcirculation data in fact provide stronger prognostic evidence than global hemodynamic parameters such as blood pressure or heart rate [9]. Global systemic hemodynamic failure, however, does not seem to correlate with microcirculatory impairment [10], and is poorly understood and is just one of the factors involved in the severity and fatality associated with septic shock. It thus seems unlikely that benefit in terms of mortality can be provided by cardiac output monitoring or the macrocirculation data of the pulse-indicated continuous cardiac output monitor. Use of bundles is recommended by the Surviving Sepsis Campaign 2012 [11]: this is what improves mortality [12]. Recent studies have indeed shown that implementing an Early Goal-Directed Therapy protocol does not reduce mortality in septic shock as compared with usual care [13,14]. However, since the work of Rivers et al [15] in 2001 and the first guidelines of the Surviving Sepsis Campaign in 2004, management has enormously progressed. Our practice has indeed been greatly influenced by these guidelines, which probably in themselves represent the current standard of care. It is recommended to monitor cardiac output in certain types of shock, for diagnostic purposes and to follow the progress of treatment, particularly for inotropes [16]. In our opinion, in case of sepsis, arterial pulse contour analysis and transpulmonary thermodilution should at present be reserved to refractory septic shock. Seeking to improve survival in septic shock by monitoring one component of hemodynamic failure seems impractical. Criteria such as mechanical ventilation time or duration of intensive care seem better adapted. N. Mottard, MD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet, 69495 Pierre Bénite, France Corresponding author E-mail address: [email protected] B. Allaouchiche, PhD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet, 69495 Pierre Bénite, France EA 4174 Sepsis Inflammation Hémostase, Vetagro Sup-Campus Vétérinaire de Lyon, 1 Avenue Bourgelat, 69280 Marcy-l'Étoile, France A. Friggeri, MD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet, 69495 Pierre Bénite, France J. Bohé, PhD V. Piriou, PhD Service de Réanimation, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, 165 chemin du grand Revoyet 69495 Pierre Bénite, France Université Claude-Bernard, Lyon 1, France
http://dx.doi.org/10.1016/j.ajem.2015.07.034
1521
References [1] Zhang Z, Ni H, Qian Z. Effectiveness of treatment based on PiCCO parameters in critically ill patients with septic shock and/or acute respiratory distress syndrome: a randomized controlled trial. Intensive Care Med 2015;41(3):444–51. [2] Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med 2013;369(9): 840–51. [3] Gattinoni L, Brazzi L, Pelosi P, Latini R, Tognoni G, Pesenti A, et al. A trial of goaloriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group. N Engl J Med 1995;333(16):1025–32. [4] Asfar P, Meziani F, Hamel J-F, Grelon F, Megarbane B, Anguel N, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014;370(17): 1583–93. [5] De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362(9):779–89. [6] Levy B, Collin S, Sennoun N, Ducrocq N, Kimmoun A, Asfar P, et al. Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside. Intensive Care Med 2010;36(12):2019–29. [7] Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock. Crit Care Med 2008;36(6): 1701–6. [8] De Backer D, Creteur J, Preiser J-C, Dubois M-J, Vincent J-L. Microvascular blood flow is altered in patients with sepsis. Am J Respir Crit Care Med 2002;166(1):98–104. [9] Ince C. The microcirculation is the motor of sepsis. Crit Care Lond Engl 2005;9(Suppl. 4): S13–9. [10] De Backer D, Creteur J, Dubois M-J, Sakr Y, Koch M, Verdant C, et al. The effects of dobutamine on microcirculatory alterations in patients with septic shock are independent of its systemic effects. Crit Care Med 2006;34(2):403–8. [11] Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock, 2012. Intensive Care Med 2013;39(2):165–228. [12] Levy MM, Dellinger RP, Townsend SR, Linde-Zwirble WT, Marshall JC, Bion J, et al. The Surviving Sepsis Campaign: results of an international guideline-based performance improvement program targeting severe sepsis. Intensive Care Med 2010; 36(2):222–31. [13] Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA, Pike F, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med 2014;370(18): 1683–93. [14] Peake SL, Delaney A, Bailey M, Bellomo R, Cameron PA, Cooper DJ, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med 2014;371(16): 1496–506. [15] Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, et al. Early goaldirected therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345(19):1368–77. [16] Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med 2014;40(12):1795–815.
Right ventricular diastolic function in patients with community-acquired pneumonia☆ To the Editor, We read with great interest the article “Is there a potential role for echocardiography in adult patients with community-acquired pneumonia? A pilot study” written by Yildirim et al [1]. They aimed to investigate left and right ventricular (RV) functions and aortic elastic properties and observe relationships between echocardiographic findings and inflammatory and cardiac serum biomarkers in communityacquired pneumonia (CAP) patients. They showed that CAP is associated with reduced levels of tricuspid annular plane systolic excursion and impaired elasticity of the ascending aorta, and these markers are correlated with the severity of the disease. We believe that these findings will act as a guide for further studies regarding echocardiographic evaluation of left and RV functions in patients with CAP. Tricuspid annular plane systolic excursion can be used routinely as a simple method of estimating RV systolic function but not diastolic function. Contrary to common belief, the right ventricle is not a passive chamber. Multiple studies have demonstrated that RV diastolic dysfunction usually occurs before apparent RV systolic dysfunction and RV dilatation. Therefore, it serves as an early and more easily quantifiable marker of subclinical RV dysfunction. A large number of acute and chronic diseases have been associated with RV diastolic dysfunction, including both pressure and volume ☆ There is no conflict of interest.
1522
Correspondence / American Journal of Emergency Medicine 33 (2015) 1515–1535
overload pathologies such as primary lung disease, congenital heart disease, cardiomyopathies, ischemic heart disease, and systemic diseases [2,3]. Right ventricular diastolic function has been evaluated using Doppler velocities of the transtricuspid flow (E, A, and E/A), tissue Doppler velocities of the tricuspid annulus (E′, A′, E′/A′), deceleration time, and isovolumic relaxation time. Most commonly used in recent studies are the tricuspid E/E′ ratio, right atrial (RA) area or volume, and diastolic strain rate. It has been shown to be a good correlation between the tricuspid E/E′ ratio and RA volume, and hemodynamic parameters. An E/E′ ratio if 4 or higher had high sensitivity and specificity for predicting RA pressure of 10 mm Hg or greater in noncardiac surgery intensive care unit patients [4]. The current study did not evaluate RV diastolic function and RA volume [1]. On the other hand, it would be better if they also evaluated RV function using other parameters including RV index of myocardial performance, myocardial acceleration during isovolumic contraction, and RV fractional area change. Because these quantitative measurement are simple and reproducible, they do not require sophisticated equipment or prolonged image analysis. We think that it might be helpful if the RV systolic and diastolic functions were assessed by using these quantitative parameters in patients with CAP in the further studies. Sait Demirkol, MD* Cengiz Ozturk, MD Sevket Balta, MD Murat Unlu, MD Zekeriya Arslan, MD Gulhane Military Medical Academy, School of Medicine Department of Cardiology, Ankara, Turkey ⁎Corresponding author at: Department of Cardiology Gulhane School of Medicine, Tevfik Saglam St, 06018 Etlik, Ankara, Turkey Tel.: +90 312 3044281; fax: +90 312 3044250 E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.07.022 References [1] Yıldırım B, Biteker FS, Basaran O, Alatas OD, Acar E, Sozen H, et al. Is there a potential role for echocardiography in adult patients with community-acquired pneumonia? A pilot study. Am J Emerg Med 2015. http://dx.doi.org/10.1016/j.ajem.2015.06.036 [Epub ahead of print]. [2] Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 2010;23:685–713. [3] Cardoso SM, Miyague NI. Right ventricular diastolic dysfunction in the postoperative period of tetralogy of Fallot. Arq Bras Cardiol 2003;80(2):198–201 [194–7]. [4] Sade LE, Gulmez O, Eroglu S, Sezgin A, Muderrisoglu H. Noninvasive estimation of right ventricular filling pressure by ratio of early tricuspid inflow to annular diastolic velocity in patients with and without recent cardiac surgery. J Am Soc Echocardiogr 2007;20:982–8.
No correlation between body size and hydromorphone analgesia in obese patients in ED
To the Editor, Obesity is associated with pain, and pain is the most common presentation in the emergency department [1,2]. The mainstay treatment
of moderate and severe pain in the emergency department is intravenous opioids, but the appropriate opioid dosing for obese patients is still in question. Due to their increased body sizes and altered fat-lean mass ratios, body size measures, such as lean body weight and ideal body weight, have been recommended and used to dose intravenous opioids in obese patients [3,4]. However, previous studies have neither confirmed nor disproved these dosing recommendations. The current study was a secondary analysis of a previously conducted prospective clinical trial in the emergency department at an academic urban hospital [5]. The study was approved by the institutional review board and registered with ClinicalTrials.gov (Identifier NCT01675778). Inclusion and exclusion criteria, as well as the study protocol, have previously been described [5]. Briefly, all study participants received 1 mg intravenous hydromorphone. Pain intensities (Numeric Rating Scale, or NRS) were collected before and 30 minutes after hydromorphone administration. Patient demographics, pain duration, location, and mechanism (injury vs noninjury) were recorded. When patients were more comfortable after the treatment, their weight (kilogram) and height (centimeter) were measured (Scale-Tronix; Scale-Tronix Inc, Carol Stream, IL). Various body size measures were calculated [6]. Scatterplots were constructed to show the relationships between different body size measures and clinical NRS changes 30 minutes after hydromorphone administration. Pearson correlation coefficients were also calculated. Statistical software STATA version 12.1 (Stata Corporation, College Station, TX) was used for data analysis. We had 73 study participants with body mass index (BMI) of 30 kg/m2 or greater. Their baseline characteristics are listed in Table. As shown in Figure, there were no statistically significant correlations between pain NRS changes and any of the body size measures examined here. The lack of the correlation between these body size measures and response to opioid analgesia may be explained by studies of opioid pharmacodynamics, which have failed to demonstrate an association between opioid plasma concentration and clinical analgesic effects [7]. Our study results do not support the recommendation to adjust hydromorphone doses based on any of the body size measures examined here. An initial fixed dose of intravenous hydromorphone should be used in obese patients with acute pain in the emergency department. Limitations to the current study included small sample size, short assessment time (30 minutes after hydromorphone administration), heterogeneous pain causes, bivariate association analysis without considering other influencing factors (sex, race, psychological, and genetic factors could also affect pain treatment response), and single-center study. In summary, the current analysis does not support adjusting opioid doses based on various body size measures in obese patients. An initial fixed dose of opioids should be used in obese patients with acute pain in the emergency department.
Shujun Xia, MD, PhD* Edward Chew, MD Dong Choe, MD Lenin Hernandez, BA Adrienne Birnbaum, MD, MS Department of Emergency Medicine, Jacobi Medical Center Albert Einstein College of Medicine, Bronx, NY *Corresponding author. Department of Emergency Medicine, Jacobi Medical Center, 1400 Pelham Parkway South, Bronx, NY 10461
Body size measures
Male
Female
BMI Ideal body weight (IBW) Lean body weight Body surface area Adjusted body weight Predicted normal weight
kg/m2 = TBW/height2 kg = 45.4 + 0.89 × [height (cm) − 152.4] + 4.5 kg = 9270 × TBW/(6680 + 216 × BMI) m2 = √[(height(cm) × TBW)/3600] kg = IBW + 0.4 × (TBW − IBW) kg = 1.57 × TBW − 0.0183 × BMI × TBW − 10.5
Same as male kg = 45.4 + 0.89 × [height (cm) − 152.4] kg = 9270 × TBW/(8780 + 244 × BMI) Same as male Same as male kg = 1.75 × TBW − 0.0242 × BMI × TBW − 12.6