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Ultrasound Corner
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A 71-Year-Old Woman Presenting With Abdominal Pain and Dyspnea Kan Liu, MD, PhD; Debanik Chaudhuri, MD; and Arunpreet Kahlon, MD
CHEST 2017; 152(4):e81-e84
A 71-year-old woman presented with sudden abnormal pain and vomiting. She underwent a CT imaging study of the abdomen, which revealed ischemic bowel perforation secondary to an incarcerated hernia (Figs 1A, 1B). An urgent surgery for acute abdomen was planned. However, the patient suddenly became dyspneic and hypotensive (systolic blood pressure, 70 mm Hg). In addition to diffuse rebound abdominal tenderness and cold extremities, there were noteworthy crackles in bilateral lung bases. A III/VI systolic murmur was heard at the left upper sternal border. A chest radiograph was therefore performed and revealed diffuse bilateral infiltrates, consistent with pulmonary edema (Fig 2A). A simultaneous ECG revealed an ST-segment elevation myocardial infarction (STEMI) pattern (Fig 2B). Other laboratory data were notable for the following: WBC count, 10.5 K/mL; lactic acid, 2.2 mmol/L; creatine, 1.9 mg/dL; creatinine kinase-MB, 31.40 ng/mL; and cardiac troponin T, 1.46 ng/mL. The surgery was postponed due to concern regarding significantly increased operative mortality in the presence of untreated STEMI. Transthoracic echocardiography (TTE) was performed (Videos 1-4).
Figure 1 – A CT imaging study of the abdomen revealed ischemic bowel perforation (A) secondary to incarcerated hernia (B).
AFFILIATIONS: From the State University of New York, Upstate Medical University, Syracuse, NY. CORRESPONDENCE TO: Kan Liu, MD, PhD, Heart and Vascular Center, State University of New York, Upstate Medical University, UHCC 5th Floor, 90 Presidential Plaza, Syracuse, NY 13202; e-mail: [email protected] Copyright Ó 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved. DOI: http://dx.doi.org/10.1016/j.chest.2017.04.190
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Figure 2 – A, A portable chest radiograph shows bilateral hilar fullness/ haziness, diffuse infiltrates, and pleural effusion. B, An ECG revealed an ST-segment elevation myocardial infarction pattern.
Question: On the basis of Videos 1 through 4, and the patient’s clinical presentation/ laboratory data, which of the following is the next best step in management? A. Thrombolytic therapy B. Cardiac catheterization with percutaneous coronary intervention C. Urgent surgery for ischemic bowel perforation D. Conservative medical management
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152#4 CHEST OCTOBER 2017
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Answer: C Discussion Combined with the clinical picture, severe ventricular dysfunction with only minimal elevations in cardiac enzyme levels is consistent with apical ballooning syndrome (or Takotsubo syndrome [TTS]). This diagnosis avoided potentially harmful treatments for STEMI and allowed life-saving surgery to be performed in a timely manner. Therefore, option C is correct. Bowel perforation/ bleeding contradict not only thrombolytic therapy but also antiplatelet/anticoagulation therapy required for cardiac catheterization/percutaneous coronary intervention. Thus, both option A and option B are wrong. Medical management cannot treat acute abdomen or prevent hypovolumic/septic shock, and thus option D is also wrong. Although the changes on the ECG were concerning for an acute myocardial infarction, there were important discriminating features of the case to allow another
diagnosis. These features included the following: (1) despite ST-segment elevation, reciprocal ECG change was lacking (Fig 2B); (2) the degree of cardiac enzyme elevation was too low for the degree of left ventricular dysfunction shown by the echocardiogram; and (3) the pattern of the ventricular contractile dysfunction in the echocardiogram (Videos 1-3) was beyond the myocardial territory of any single coronary artery. In addition, apical (hypokinetic) and basal (hyperkinetic) segments exhibited a discordant contractile pattern (Figs 3A, 3B). These findings support the diagnosis of TTS. TTS also caused a dynamic left ventricular outflow tract (LVOT) obstruction, generating the systolic murmur and resulting in hypotension (Figs 3C, 3D, Video 4). Of note, catecholamine inotropes/vasopressors are harmful because they can worsen LVOT obstruction and hemodynamic instability. After we provided prompt fluid resuscitation and IV phenylephrine infusion, the patient became hemodynamically stable and underwent successful exploratory laparotomy/small
Figure 3 – A, A two-dimensional echocardiogram revealed apical akinesis (arrowheads) in an apical two-chamber view. B, A speckle-tracking echocardiogram depicts a unique distribution pattern of abnormal myocardial contractility in a left ventricular 17-segment (bull’s eye) plot. Impaired peak systolic longitudinal strains are highlighted by digital (normal, –17% or lower) and color (red, normal; pink, impaired; blue, significantly impaired) codes. C, A color Doppler study shows a turbulent flow in the left ventricular outflow tract (arrowhead) and simultaneous mitral regurgitation (arrow). D, A continuous-wave Doppler study shows an increased gradient across the left ventricular outflow tract (arrowhead, the first heart beat) and mitral regurgitation (arrow, the second heart beat).
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bowel excision. The ECG and echocardiographic abnormalities spontaneously normalized in 3 weeks. TTS often mimics the clinical features of acute myocardial infarction, including STEMI. Coronary angiography is the only definitive approach to differentiate TTS and acute myocardial infarction.1,2 Nevertheless, frontline clinicians often face a dilemma when cardiac catheterization and thrombolytic therapy (in case of STEMI) is contradicted or can potentially cause critical adverse consequences. Under lifethreatening conditions, characteristic ECG/noninvasive imaging features can provide valuable diagnostic information to prompt timely decision-making. Although most TTS episodes have a benign course, acute heart failure and hemodynamic instability can occur.3 With basal interventricular septal hypertrophy, hypercontractility of basilar walls and systolic anterior motion of the anterior leaflet of the mitral valve can induce dynamic LVOT obstruction, disrupting coaptation of the mitral valve and worsening mitral regurgitation.4 Avoiding catecholamine inotropes/ pressors (eg, dobutamine), maintaining appropriate ventricular preload, and applying alpha-adrenergic agonists (when indicated) might be the most effective therapies during the acute phase of TTS.
Reverberations 1. TTS often mimics clinical and ECG features of acute anterior myocardial infarction.
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2. When cardiac catheterization is contradicted, characteristic noninvasive imaging characteristics can provide valuable diagnostic information to help timely decision-making under life-threatening conditions. 3. Dynamic LVOT obstruction and mitral regurgitation play important roles in the development of heart failure and hemodynamic instability during episodes of TTS (Discussion Video).
Acknowledgments Author contributions: K. L., D. C., and A. K. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis, including and especially any adverse effects. K. L., D. C., and A. K. helped write the manuscript. Financial/nonfinancial disclosures: None declared. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online version of this article.
References 1. Lyon AR, Bossone E, Schneider B, et al. Current state of knowledge on Takotsubo syndrome: a position statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2016;18(1):8-27. 2. Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy. N Engl J Med. 2015;373(10):929-938. 3. Citro R, Rigo F, D’Andrea A, et al. Echocardiographic correlates of acute heart failure, cardiogenic shock, and in-hospital mortality in tako-tsubo cardiomyopathy. JACC Cardiovasc Imaging. 2014;7(2): 119-129. 4. Liu K, Krone JK. What truly causes the adverse outcome of Tako-Tsubo cardiomyopathy? JACC Cardiovasc Imaging. 2014;7(7):742-743.
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152#4 CHEST OCTOBER 2017
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Ultrasound Corner
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A 71-Year-Old Woman Presenting With Abdominal Pain and Dyspnea Kan Liu, MD, PhD; Debanik Chaudhuri, MD; and Arunpreet Kahlon, MD
CHEST 2017; 152(4):e81-e84
A 71-year-old woman presented with sudden abnormal pain and vomiting. She underwent a CT imaging study of the abdomen, which revealed ischemic bowel perforation secondary to an incarcerated hernia (Figs 1A, 1B). An urgent surgery for acute abdomen was planned. However, the patient suddenly became dyspneic and hypotensive (systolic blood pressure, 70 mm Hg). In addition to diffuse rebound abdominal tenderness and cold extremities, there were noteworthy crackles in bilateral lung bases. A III/VI systolic murmur was heard at the left upper sternal border. A chest radiograph was therefore performed and revealed diffuse bilateral infiltrates, consistent with pulmonary edema (Fig 2A). A simultaneous ECG revealed an ST-segment elevation myocardial infarction (STEMI) pattern (Fig 2B). Other laboratory data were notable for the following: WBC count, 10.5 K/mL; lactic acid, 2.2 mmol/L; creatine, 1.9 mg/dL; creatinine kinase-MB, 31.40 ng/mL; and cardiac troponin T, 1.46 ng/mL. The surgery was postponed due to concern regarding significantly increased operative mortality in the presence of untreated STEMI. Transthoracic echocardiography (TTE) was performed (Videos 1-4).
Figure 1 – A CT imaging study of the abdomen revealed ischemic bowel perforation (A) secondary to incarcerated hernia (B).
AFFILIATIONS: From the State University of New York, Upstate Medical University, Syracuse, NY. CORRESPONDENCE TO: Kan Liu, MD, PhD, Heart and Vascular Center, State University of New York, Upstate Medical University, UHCC 5th Floor, 90 Presidential Plaza, Syracuse, NY 13202; e-mail: [email protected] Copyright Ó 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved. DOI: http://dx.doi.org/10.1016/j.chest.2017.04.190
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Figure 2 – A, A portable chest radiograph shows bilateral hilar fullness/ haziness, diffuse infiltrates, and pleural effusion. B, An ECG revealed an ST-segment elevation myocardial infarction pattern.
Question: On the basis of Videos 1 through 4, and the patient’s clinical presentation/ laboratory data, which of the following is the next best step in management? A. Thrombolytic therapy B. Cardiac catheterization with percutaneous coronary intervention C. Urgent surgery for ischemic bowel perforation D. Conservative medical management
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152#4 CHEST OCTOBER 2017
]
Answer: C Discussion Combined with the clinical picture, severe ventricular dysfunction with only minimal elevations in cardiac enzyme levels is consistent with apical ballooning syndrome (or Takotsubo syndrome [TTS]). This diagnosis avoided potentially harmful treatments for STEMI and allowed life-saving surgery to be performed in a timely manner. Therefore, option C is correct. Bowel perforation/ bleeding contradict not only thrombolytic therapy but also antiplatelet/anticoagulation therapy required for cardiac catheterization/percutaneous coronary intervention. Thus, both option A and option B are wrong. Medical management cannot treat acute abdomen or prevent hypovolumic/septic shock, and thus option D is also wrong. Although the changes on the ECG were concerning for an acute myocardial infarction, there were important discriminating features of the case to allow another
diagnosis. These features included the following: (1) despite ST-segment elevation, reciprocal ECG change was lacking (Fig 2B); (2) the degree of cardiac enzyme elevation was too low for the degree of left ventricular dysfunction shown by the echocardiogram; and (3) the pattern of the ventricular contractile dysfunction in the echocardiogram (Videos 1-3) was beyond the myocardial territory of any single coronary artery. In addition, apical (hypokinetic) and basal (hyperkinetic) segments exhibited a discordant contractile pattern (Figs 3A, 3B). These findings support the diagnosis of TTS. TTS also caused a dynamic left ventricular outflow tract (LVOT) obstruction, generating the systolic murmur and resulting in hypotension (Figs 3C, 3D, Video 4). Of note, catecholamine inotropes/vasopressors are harmful because they can worsen LVOT obstruction and hemodynamic instability. After we provided prompt fluid resuscitation and IV phenylephrine infusion, the patient became hemodynamically stable and underwent successful exploratory laparotomy/small
Figure 3 – A, A two-dimensional echocardiogram revealed apical akinesis (arrowheads) in an apical two-chamber view. B, A speckle-tracking echocardiogram depicts a unique distribution pattern of abnormal myocardial contractility in a left ventricular 17-segment (bull’s eye) plot. Impaired peak systolic longitudinal strains are highlighted by digital (normal, –17% or lower) and color (red, normal; pink, impaired; blue, significantly impaired) codes. C, A color Doppler study shows a turbulent flow in the left ventricular outflow tract (arrowhead) and simultaneous mitral regurgitation (arrow). D, A continuous-wave Doppler study shows an increased gradient across the left ventricular outflow tract (arrowhead, the first heart beat) and mitral regurgitation (arrow, the second heart beat).
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bowel excision. The ECG and echocardiographic abnormalities spontaneously normalized in 3 weeks. TTS often mimics the clinical features of acute myocardial infarction, including STEMI. Coronary angiography is the only definitive approach to differentiate TTS and acute myocardial infarction.1,2 Nevertheless, frontline clinicians often face a dilemma when cardiac catheterization and thrombolytic therapy (in case of STEMI) is contradicted or can potentially cause critical adverse consequences. Under lifethreatening conditions, characteristic ECG/noninvasive imaging features can provide valuable diagnostic information to prompt timely decision-making. Although most TTS episodes have a benign course, acute heart failure and hemodynamic instability can occur.3 With basal interventricular septal hypertrophy, hypercontractility of basilar walls and systolic anterior motion of the anterior leaflet of the mitral valve can induce dynamic LVOT obstruction, disrupting coaptation of the mitral valve and worsening mitral regurgitation.4 Avoiding catecholamine inotropes/ pressors (eg, dobutamine), maintaining appropriate ventricular preload, and applying alpha-adrenergic agonists (when indicated) might be the most effective therapies during the acute phase of TTS.
Reverberations 1. TTS often mimics clinical and ECG features of acute anterior myocardial infarction.
e84 Ultrasound Corner
2. When cardiac catheterization is contradicted, characteristic noninvasive imaging characteristics can provide valuable diagnostic information to help timely decision-making under life-threatening conditions. 3. Dynamic LVOT obstruction and mitral regurgitation play important roles in the development of heart failure and hemodynamic instability during episodes of TTS (Discussion Video).
Acknowledgments Author contributions: K. L., D. C., and A. K. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis, including and especially any adverse effects. K. L., D. C., and A. K. helped write the manuscript. Financial/nonfinancial disclosures: None declared. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online version of this article.
References 1. Lyon AR, Bossone E, Schneider B, et al. Current state of knowledge on Takotsubo syndrome: a position statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2016;18(1):8-27. 2. Templin C, Ghadri JR, Diekmann J, et al. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy. N Engl J Med. 2015;373(10):929-938. 3. Citro R, Rigo F, D’Andrea A, et al. Echocardiographic correlates of acute heart failure, cardiogenic shock, and in-hospital mortality in tako-tsubo cardiomyopathy. JACC Cardiovasc Imaging. 2014;7(2): 119-129. 4. Liu K, Krone JK. What truly causes the adverse outcome of Tako-Tsubo cardiomyopathy? JACC Cardiovasc Imaging. 2014;7(7):742-743.
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152#4 CHEST OCTOBER 2017
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