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Obesity and Cardiopulmonary BypassAssociated Acute Kidney Injury: Authors’ Reply To the Editor: We thank Xue et al for their time and interest in our study titled, “Obesity and Post-Cardiopulmonary Bypass-Associated Acute Kidney Injury: A Single-Center Retrospective Analysis.” The authors correctly noted the role of numerous risk factors for acute kidney injury following cardiopulmonary bypass (AKI-CPB). Our retrospective analysis of 376 patients who underwent cardiac surgery with cardiopulmonary bypass was completed in an academic medical center in the United States. AKI-CPB has a multifactorial etiology and cannot be explained satisfactorily by a “single-hit” hypothesis. In the last 15 years, there have been more than 15 major and minor risk factors for AKI-CPB, multiple predictive models, scoring systems, biomarkers of AKI-CPB described in the literature.1,2 The limitation of any retrospective analysis is the availability of viable data and a large enough data set to account for every single risk factor that is described for a particular entity. Our study is no exception. As mentioned in our method section, the association of the demographic, preoperative, intraoperative, and postoperative variables with AKI-CPB was tested. The variables that were statistically different between the AKI and No AKI cohorts, and variables associated with AKICPB between body mass index (BMI) classes were used as covariates in a multivariate logistic regression model to assess the effect of BMI on AKI-CPB, while controlling for covariates. There has been a renewed focus on preoperative anemia as a risk factor for AKI-CPB since the publication by Karkouti et al.3 In our study, we used the preoperative transfusion as a surrogate marker for hemodynamically significant preoperative anemia. The decision to transfuse the patients preoperatively was made by the attending anesthesiologist or surgeon. We acknowledge that this surrogate measure may not encompass the entire complexity of preoperative anemia. There was no statistically significant difference between the AKI-CPB and No-AKI cohorts based on the need for preoperative transfusion support. We agree that intraoperative hemodynamics have a significant role to play in the pathophysiology of AKI-CPB. Our team of experienced cardiac anesthesiologists does an excellent job of managing these incredibly complex patients. In our data set, the AKI-CPB cohort had a mean CPB time of 122 minutes (101-175 min IQR) IQR and the cohort who did not develop AKI-CPB had a mean CPB time of 106 minutes (88-141 min IQR). In the cohort that went on to develop AKI-CPB with extended CPB times of greater than 150 minutes were also those who needed more hemodynamic modulation with vasoactive medications in the intraoperative period. They were supported hemodynamically with varying combinations of epinephrine, norepinephrine, phenylephrine, milrinone, dobutamine, fluids and transfusion support. Because of the dynamic nature and constant changes in intraoperative dosing, we had data on individual exposure to various agents and not the minute-to-minute dosing of the medications. This cohort of
LETTERS TO THE EDITOR
hemodynamically unstable patients also received more transfusion support. Interestingly the mean BMI of this cohort was 30 ⫾ 8. Evidence-based practice and especially, adherence to the nationally described guidelines for management of patients on CPB, are the norm at the parent institution. The current practice at our institution is in accordance with these guidelines and a prudent transfusion trigger is at a hematocrit of 21 to 24.4 There has been a focus on the modifiable risk factors in preventing AKI-CPB. This is especially true after the early publications of the pleotropic effects of HMG-CoA reductase inhibitors or statins on kidney function. The present day data on statins and the prevention of AKI-CPB are unclear, with several studies falling equally on the pro and con spectrum of discussion.5–7 In our study, we included established risk factors and did not include the exposure of statins in the perioperative period. Overall, we acknowledge the thoughtful letter of Xue et al regarding our study focusing on the role of obesity and AKI-CPB. The merit of our study was the robust but moderate sized data set that spanned 4 years, multiple cardiac anesthesiologists and at least 5 cardiac surgeons. Our retrospective data set had limitations that cannot account for all combinations of risk factors for AKI-CPB. The effects of unmeasured confounders on these relationships, therefore, cannot be dismissed. ACKNOWLEDGMENTS Departmental funding only.
Avinash B. Kumar, MD, FCCP, FCCM* M. Bridget Zimmerman, PhD† Manish Suneja, MD‡ *Department of Anesthesia Division of Critical Care Vanderbilt University Nashville, TN †Department of Biostatistics University of Iowa Iowa City, IA ‡Department of Nephrology University of Iowa Hospitals and Clinics Iowa City, IA
REFERENCES 1. Huen SC, Parikh CR: Predicting acute kidney injury after cardiac surgery: a systematic review. Ann Thorac Surg 93:337-347, 2012 2. Kumar AB, Suneja M: Cardiopulmonary bypass-associated acute kidney injury. Anesthesiology 114:964-970, 2011 3. Karkouti K, Wijeysundera DN, Yau TM, et al: Influence of erythrocyte transfusion on the risk of acute kidney injury after cardiac surgery differs in anemic and nonanemic patients. Anesthesiology 115: 523-530, 2011 4. Society of Thoracic Surgeons Blood Conservation Guideline Task F, Ferraris VA, Ferraris SP, et al: Perioperative blood transfusion and blood conservation in cardiac surgery: the Society of Thoracic Surgeons and The Society of Cardiovascular Anesthesiologists clinical practice guideline. Ann Thorac Surg 83:S27-S86, 2007
LETTERS TO THE EDITOR
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5. Mithani S, Kuskowski M, Slinin Y, et al: Dose-dependent effect of statins on the incidence of acute kidney injury after cardiac surgery. Ann Thorac Surg 91:520-525, 2011 6. Molnar AO, Parikh CR, Coca SG, et al: Association between preoperative statin use and acute kidney injury biomarkers in cardiac surgical procedures. Ann Thorac Surg 97:2081-2087, 2014 7. Prowle JR, Calzavacca P, Licari E, et al: Pilot double-blind, randomized controlled trial of short-term atorvastatin for prevention of acute kidney injury after cardiac surgery. Nephrology 17:215-224, 2012 http://dx.doi.org/10.1053/j.jvca.2014.08.016
Apical Thrombus After Pericardiectomy for Constrictive Pericarditis To the Editor: Chronic constriction leads to myocardial damage. Following pericardiectomy, cardiac dysfunction may occur in one-third of
Fig 1.
patients as a consequence of the rapid increase in left ventricle (LV) volume and abrupt changes in LV geometry.1,2 While severe LV dysfunction may lead to the development of apical mural thrombus, such a complication has been described only once after decortication.3 In this regard, we are not confident that low-cardiac-output syndrome (LCOS) is the sole underlying mechanism. We report the case of a 48-year-old woman with preserved systolic function and normal coronary angiography who underwent standard “phrenic-to-phrenic” pericardiectomy. The procedure was achieved without cardiopulmonary bypass through a full median sternotomy. The patient experienced severe postoperative LCOS. The left ventricular ejection fraction was estimated to be 25%. Regional wall motion abnormalities predominated in mid-and apical LV segments. However, cardiac enzymes were negative. The LCOS was managed successfully with inotropic and vasopressive support. Transthoracic echocardiography on the 8th postoperative day revealed, on one hand, a significant improvement of the left ventricular ejection fraction (E 45%) despite the persistent akinesia of the apex, and, on the other hand, the appearance of a hyperechogenic apical mass (Fig 1A). Magnetic resonance imaging (MRI) was strongly suggestive of an apical thrombus measuring about 4 cm. Moreover, MRI data revealed the persistence of some islands of thick pericardium facing the apex (Fig 1B).
(A) TTE views showing the LV apical thrombus (arrows). (B) Magnetic resonance imaging slices showing the LV apical thrombus (arrows).
Obesity and Cardiopulmonary BypassAssociated Acute Kidney Injury: Authors’ Reply To the Editor: We thank Xue et al for their time and interest in our study titled, “Obesity and Post-Cardiopulmonary Bypass-Associated Acute Kidney Injury: A Single-Center Retrospective Analysis.” The authors correctly noted the role of numerous risk factors for acute kidney injury following cardiopulmonary bypass (AKI-CPB). Our retrospective analysis of 376 patients who underwent cardiac surgery with cardiopulmonary bypass was completed in an academic medical center in the United States. AKI-CPB has a multifactorial etiology and cannot be explained satisfactorily by a “single-hit” hypothesis. In the last 15 years, there have been more than 15 major and minor risk factors for AKI-CPB, multiple predictive models, scoring systems, biomarkers of AKI-CPB described in the literature.1,2 The limitation of any retrospective analysis is the availability of viable data and a large enough data set to account for every single risk factor that is described for a particular entity. Our study is no exception. As mentioned in our method section, the association of the demographic, preoperative, intraoperative, and postoperative variables with AKI-CPB was tested. The variables that were statistically different between the AKI and No AKI cohorts, and variables associated with AKICPB between body mass index (BMI) classes were used as covariates in a multivariate logistic regression model to assess the effect of BMI on AKI-CPB, while controlling for covariates. There has been a renewed focus on preoperative anemia as a risk factor for AKI-CPB since the publication by Karkouti et al.3 In our study, we used the preoperative transfusion as a surrogate marker for hemodynamically significant preoperative anemia. The decision to transfuse the patients preoperatively was made by the attending anesthesiologist or surgeon. We acknowledge that this surrogate measure may not encompass the entire complexity of preoperative anemia. There was no statistically significant difference between the AKI-CPB and No-AKI cohorts based on the need for preoperative transfusion support. We agree that intraoperative hemodynamics have a significant role to play in the pathophysiology of AKI-CPB. Our team of experienced cardiac anesthesiologists does an excellent job of managing these incredibly complex patients. In our data set, the AKI-CPB cohort had a mean CPB time of 122 minutes (101-175 min IQR) IQR and the cohort who did not develop AKI-CPB had a mean CPB time of 106 minutes (88-141 min IQR). In the cohort that went on to develop AKI-CPB with extended CPB times of greater than 150 minutes were also those who needed more hemodynamic modulation with vasoactive medications in the intraoperative period. They were supported hemodynamically with varying combinations of epinephrine, norepinephrine, phenylephrine, milrinone, dobutamine, fluids and transfusion support. Because of the dynamic nature and constant changes in intraoperative dosing, we had data on individual exposure to various agents and not the minute-to-minute dosing of the medications. This cohort of
LETTERS TO THE EDITOR
hemodynamically unstable patients also received more transfusion support. Interestingly the mean BMI of this cohort was 30 ⫾ 8. Evidence-based practice and especially, adherence to the nationally described guidelines for management of patients on CPB, are the norm at the parent institution. The current practice at our institution is in accordance with these guidelines and a prudent transfusion trigger is at a hematocrit of 21 to 24.4 There has been a focus on the modifiable risk factors in preventing AKI-CPB. This is especially true after the early publications of the pleotropic effects of HMG-CoA reductase inhibitors or statins on kidney function. The present day data on statins and the prevention of AKI-CPB are unclear, with several studies falling equally on the pro and con spectrum of discussion.5–7 In our study, we included established risk factors and did not include the exposure of statins in the perioperative period. Overall, we acknowledge the thoughtful letter of Xue et al regarding our study focusing on the role of obesity and AKI-CPB. The merit of our study was the robust but moderate sized data set that spanned 4 years, multiple cardiac anesthesiologists and at least 5 cardiac surgeons. Our retrospective data set had limitations that cannot account for all combinations of risk factors for AKI-CPB. The effects of unmeasured confounders on these relationships, therefore, cannot be dismissed. ACKNOWLEDGMENTS Departmental funding only.
Avinash B. Kumar, MD, FCCP, FCCM* M. Bridget Zimmerman, PhD† Manish Suneja, MD‡ *Department of Anesthesia Division of Critical Care Vanderbilt University Nashville, TN †Department of Biostatistics University of Iowa Iowa City, IA ‡Department of Nephrology University of Iowa Hospitals and Clinics Iowa City, IA
REFERENCES 1. Huen SC, Parikh CR: Predicting acute kidney injury after cardiac surgery: a systematic review. Ann Thorac Surg 93:337-347, 2012 2. Kumar AB, Suneja M: Cardiopulmonary bypass-associated acute kidney injury. Anesthesiology 114:964-970, 2011 3. Karkouti K, Wijeysundera DN, Yau TM, et al: Influence of erythrocyte transfusion on the risk of acute kidney injury after cardiac surgery differs in anemic and nonanemic patients. Anesthesiology 115: 523-530, 2011 4. Society of Thoracic Surgeons Blood Conservation Guideline Task F, Ferraris VA, Ferraris SP, et al: Perioperative blood transfusion and blood conservation in cardiac surgery: the Society of Thoracic Surgeons and The Society of Cardiovascular Anesthesiologists clinical practice guideline. Ann Thorac Surg 83:S27-S86, 2007
LETTERS TO THE EDITOR
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5. Mithani S, Kuskowski M, Slinin Y, et al: Dose-dependent effect of statins on the incidence of acute kidney injury after cardiac surgery. Ann Thorac Surg 91:520-525, 2011 6. Molnar AO, Parikh CR, Coca SG, et al: Association between preoperative statin use and acute kidney injury biomarkers in cardiac surgical procedures. Ann Thorac Surg 97:2081-2087, 2014 7. Prowle JR, Calzavacca P, Licari E, et al: Pilot double-blind, randomized controlled trial of short-term atorvastatin for prevention of acute kidney injury after cardiac surgery. Nephrology 17:215-224, 2012 http://dx.doi.org/10.1053/j.jvca.2014.08.016
Apical Thrombus After Pericardiectomy for Constrictive Pericarditis To the Editor: Chronic constriction leads to myocardial damage. Following pericardiectomy, cardiac dysfunction may occur in one-third of
Fig 1.
patients as a consequence of the rapid increase in left ventricle (LV) volume and abrupt changes in LV geometry.1,2 While severe LV dysfunction may lead to the development of apical mural thrombus, such a complication has been described only once after decortication.3 In this regard, we are not confident that low-cardiac-output syndrome (LCOS) is the sole underlying mechanism. We report the case of a 48-year-old woman with preserved systolic function and normal coronary angiography who underwent standard “phrenic-to-phrenic” pericardiectomy. The procedure was achieved without cardiopulmonary bypass through a full median sternotomy. The patient experienced severe postoperative LCOS. The left ventricular ejection fraction was estimated to be 25%. Regional wall motion abnormalities predominated in mid-and apical LV segments. However, cardiac enzymes were negative. The LCOS was managed successfully with inotropic and vasopressive support. Transthoracic echocardiography on the 8th postoperative day revealed, on one hand, a significant improvement of the left ventricular ejection fraction (E 45%) despite the persistent akinesia of the apex, and, on the other hand, the appearance of a hyperechogenic apical mass (Fig 1A). Magnetic resonance imaging (MRI) was strongly suggestive of an apical thrombus measuring about 4 cm. Moreover, MRI data revealed the persistence of some islands of thick pericardium facing the apex (Fig 1B).
(A) TTE views showing the LV apical thrombus (arrows). (B) Magnetic resonance imaging slices showing the LV apical thrombus (arrows).
