DIAGNOSTIC DILEMMA
An Unexpected Finding Complicating Pericardial Effusion and Tamponade Gianluca Santise, MD,* Sergio Sciacca, MD,* Cettina Ruperto, MD,† Giovanni Gentile, MD,‡ Giovanna Panarello, MD,§ and Fabrizio Follis, MD*
A
69-YEAR-OLD WOMAN with a history of diabetes, diffuse joint pain, and previous left anterior descending coronary artery angioplasty was admitted to a community hospital with low-grade fever (37.51C) and vague chest pain associated with respiratory movements. The erythrocyte sedimentation rate and C-reactive protein were both elevated. The cardiac enzymes were normal. The electrocardiogram showed 1.5-mm ST-segment elevation in leads I, aVL, and V3 to V6. An initial transthoracic echocardiogram (TTE) showed a small pericardial effusion (0.8 cm). Suspecting an inflammatory pericarditis, the patient was treated with indomethacin, 50 mg twice a day. Three days later, the patient suffered an episode of orthostatic hypotension with nausea. A followup TTE showed worsening of the pericardial effusion (1.8 cm on the anterior wall, 1.7 cm on the lateral one), traces of fibrin, and collapse of the right atrium. The patient was urgently sent to the authors’ institution with a diagnosis of cardiac tamponade due to inflammatory pericarditis. Upon admission to the authors’ institution, the white blood cell count was 16,000 cells/µL. Another TTE confirmed the cardiac tamponade (Fig 1), and the patient was transported to the operating room for subxiphoid pericardial window during which 350 mL of serous fluid and fibrin adhesions were removed. Postoperatively, the patient remained hemodynamically stable and denied further pain. The white blood cell count rapidly
returned to the normal range, and a TTE examination conducted before the patient was discharged from the hospital excluded pericardial effusion. Pathology confirmed the diagnosis of nonspecific pericarditis. The patient returned to the referring hospital to complete the rheumatologic diagnostic workup and physical rehabilitation on the sixth postoperative day. A week later, the authors were consulted again because of purulent drainage from the surgical wound with fever, an elevated white blood cell count, and blood culture positive for methicillin-resistant Staphylococcus aureus (MRSA). In order to define mediastinal involvement, a computed tomography (CT) scan was obtained (Fig 2). What is the diagnosis?
From the *Cardiothoracic Surgery Unit, †Cardiology Unit, ‡Radiology Department, and §Anesthesiology Department, Mediterranean Institute for Transplantations and Highly Specialized Therapies, ISMETT, Palermo, Italy. Address reprint requests to Gianluca Santise, MD, Via Tricomi 1, 80127 Palermo, Italy. E-mail: [email protected] © 2014 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2014.02.009 Key words: pericardial effusion, acute aortic syndrome, echocardiography, computer tomography
Fig 1. Transthoracic echocardiogram showing the pericardial effusion (arrow). (A) Apical four-chambers long-axis view. (B) Short-axis view. (Color version of figure is available online.)
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Journal of Cardiothoracic and Vascular Anesthesia, Vol 28, No 4 (August), 2014: pp 1186–1188
UNEXPECTED FINDING COMPLICATING PERICARDIAL EFFUSION
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Fig 2. Contrast CT scan showing the pseudoaneurysm originating from the distal ascending aorta near the origin of the innominate artery (arrow). A huge hematoma is surrounding the pseudoaneurysm. (A) Axial view. (B) Sagittal view.
DIAGNOSIS: RUPTURE OF A PENETRATING ATHEROSCLEROTIC ULCER ADJACENT TO THE ORIGIN OF THE INNOMINATE ARTERY
The CT scan clearly showed a pseudoaneurysm originating from the take-off of the innominate artery and a hematoma surrounding the entire ascending aorta. A new TTE was performed specifically investigating the aortic arch (Fig 3), and the suprasternal view showed the aortic pseudoaneurysm with evidence of internal blood flow. The patient underwent an ascending aortic replacement during deep hypothermic circulatory arrest. Antegrade cerebral perfusion was provided through the right axillary artery. The intraoperative transesophageal echocardiogram confirmed the diagnosis. The pseudoaneurysm, clearly originating from an atherosclerotic ulcer rupture right by the brachiocephalic trunk and not related to the wound infection, was excluded, and the hematoma was drained. Considering such clear gross anatomy and the absence of local infection, no samples were sent to pathology or microbiology. Nevertheless, as a secondary finding, a purulent collection over the diaphragm and on the right ventricle was drained. The deep wound infection
clearly was not the cause of the pseudoaneurysm; a separate pathologic process was the cause. Several samples were sent to microbiology and grew MRSA and Enterococcus faecium. Unfortunately, despite the drainage and the lavage of the mediastinum, the patient developed sternal wound dehiscence with mediastinitis due to MRSA and episodes of septic shock with bacteremia (E. faecium, MRSA and K. pneumonia) which required sternectomy and irrigation of the mediastinum. Despite maximal medical therapy, she succumbed to sepsis thirty days after surgery. Penetrating aortic ulcer is a complication of an atherosclerotic plaque: The intima is disrupted, and the blood invades the media. It is considered an acute aortic syndrome because it can evolve to intramural hematoma, aortic dissection, or rupture.1 The clinical presentation of acute aortic syndrome can vary from typical symptoms like intense and sharp chest pain to a variety of symptoms including hypotension, dizziness or dyspnea and can be complicated by myocardial infarction, cardiac tamponade, paraplegia, and stroke. Echocardiography and CT are the most frequent imaging techniques used to establish the diagnosis in acute aortic syndrome. Echocardiography may be less sensitive
Fig 3. Transthoracic echocardiogram showing a hematoma adjacent to the innominate artery (arrow). Suprasternal view. (A) 2D view of the aortic arch. (B) Aortic arch view with color flow in the hematoma, confirming the presence of the pseudoaneurysm. (Color version of figure is available online.)
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(59%-83%) and less specific (63%-93%) than spiral CT in this setting, and the latter technique has been proposed as gold standard in case of suspected acute aortic syndrome.2,3 Indeed, in
atypical cases such as described here, echocardiography may be unable to establish the diagnosis unless there is a high index of suspicion for distal ascending aortic pathology.
REFERENCES 1. Chiu KW, Lakshminarayan R, Ettles DF: Acute aortic syndrome: CT findings. Clin Radiol 68:741-748, 2013 2. Sheikh AS, Ali K, Mazhar S: Acute Aortic Syndrome. Circulation 128:1122-1127, 2013
3. Hagan PG, Nienaber CA, Isselbacher EM, et al: The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA 283:897-903, 2000
An Unexpected Finding Complicating Pericardial Effusion and Tamponade Gianluca Santise, MD,* Sergio Sciacca, MD,* Cettina Ruperto, MD,† Giovanni Gentile, MD,‡ Giovanna Panarello, MD,§ and Fabrizio Follis, MD*
A
69-YEAR-OLD WOMAN with a history of diabetes, diffuse joint pain, and previous left anterior descending coronary artery angioplasty was admitted to a community hospital with low-grade fever (37.51C) and vague chest pain associated with respiratory movements. The erythrocyte sedimentation rate and C-reactive protein were both elevated. The cardiac enzymes were normal. The electrocardiogram showed 1.5-mm ST-segment elevation in leads I, aVL, and V3 to V6. An initial transthoracic echocardiogram (TTE) showed a small pericardial effusion (0.8 cm). Suspecting an inflammatory pericarditis, the patient was treated with indomethacin, 50 mg twice a day. Three days later, the patient suffered an episode of orthostatic hypotension with nausea. A followup TTE showed worsening of the pericardial effusion (1.8 cm on the anterior wall, 1.7 cm on the lateral one), traces of fibrin, and collapse of the right atrium. The patient was urgently sent to the authors’ institution with a diagnosis of cardiac tamponade due to inflammatory pericarditis. Upon admission to the authors’ institution, the white blood cell count was 16,000 cells/µL. Another TTE confirmed the cardiac tamponade (Fig 1), and the patient was transported to the operating room for subxiphoid pericardial window during which 350 mL of serous fluid and fibrin adhesions were removed. Postoperatively, the patient remained hemodynamically stable and denied further pain. The white blood cell count rapidly
returned to the normal range, and a TTE examination conducted before the patient was discharged from the hospital excluded pericardial effusion. Pathology confirmed the diagnosis of nonspecific pericarditis. The patient returned to the referring hospital to complete the rheumatologic diagnostic workup and physical rehabilitation on the sixth postoperative day. A week later, the authors were consulted again because of purulent drainage from the surgical wound with fever, an elevated white blood cell count, and blood culture positive for methicillin-resistant Staphylococcus aureus (MRSA). In order to define mediastinal involvement, a computed tomography (CT) scan was obtained (Fig 2). What is the diagnosis?
From the *Cardiothoracic Surgery Unit, †Cardiology Unit, ‡Radiology Department, and §Anesthesiology Department, Mediterranean Institute for Transplantations and Highly Specialized Therapies, ISMETT, Palermo, Italy. Address reprint requests to Gianluca Santise, MD, Via Tricomi 1, 80127 Palermo, Italy. E-mail: [email protected] © 2014 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2014.02.009 Key words: pericardial effusion, acute aortic syndrome, echocardiography, computer tomography
Fig 1. Transthoracic echocardiogram showing the pericardial effusion (arrow). (A) Apical four-chambers long-axis view. (B) Short-axis view. (Color version of figure is available online.)
1186
Journal of Cardiothoracic and Vascular Anesthesia, Vol 28, No 4 (August), 2014: pp 1186–1188
UNEXPECTED FINDING COMPLICATING PERICARDIAL EFFUSION
1187
Fig 2. Contrast CT scan showing the pseudoaneurysm originating from the distal ascending aorta near the origin of the innominate artery (arrow). A huge hematoma is surrounding the pseudoaneurysm. (A) Axial view. (B) Sagittal view.
DIAGNOSIS: RUPTURE OF A PENETRATING ATHEROSCLEROTIC ULCER ADJACENT TO THE ORIGIN OF THE INNOMINATE ARTERY
The CT scan clearly showed a pseudoaneurysm originating from the take-off of the innominate artery and a hematoma surrounding the entire ascending aorta. A new TTE was performed specifically investigating the aortic arch (Fig 3), and the suprasternal view showed the aortic pseudoaneurysm with evidence of internal blood flow. The patient underwent an ascending aortic replacement during deep hypothermic circulatory arrest. Antegrade cerebral perfusion was provided through the right axillary artery. The intraoperative transesophageal echocardiogram confirmed the diagnosis. The pseudoaneurysm, clearly originating from an atherosclerotic ulcer rupture right by the brachiocephalic trunk and not related to the wound infection, was excluded, and the hematoma was drained. Considering such clear gross anatomy and the absence of local infection, no samples were sent to pathology or microbiology. Nevertheless, as a secondary finding, a purulent collection over the diaphragm and on the right ventricle was drained. The deep wound infection
clearly was not the cause of the pseudoaneurysm; a separate pathologic process was the cause. Several samples were sent to microbiology and grew MRSA and Enterococcus faecium. Unfortunately, despite the drainage and the lavage of the mediastinum, the patient developed sternal wound dehiscence with mediastinitis due to MRSA and episodes of septic shock with bacteremia (E. faecium, MRSA and K. pneumonia) which required sternectomy and irrigation of the mediastinum. Despite maximal medical therapy, she succumbed to sepsis thirty days after surgery. Penetrating aortic ulcer is a complication of an atherosclerotic plaque: The intima is disrupted, and the blood invades the media. It is considered an acute aortic syndrome because it can evolve to intramural hematoma, aortic dissection, or rupture.1 The clinical presentation of acute aortic syndrome can vary from typical symptoms like intense and sharp chest pain to a variety of symptoms including hypotension, dizziness or dyspnea and can be complicated by myocardial infarction, cardiac tamponade, paraplegia, and stroke. Echocardiography and CT are the most frequent imaging techniques used to establish the diagnosis in acute aortic syndrome. Echocardiography may be less sensitive
Fig 3. Transthoracic echocardiogram showing a hematoma adjacent to the innominate artery (arrow). Suprasternal view. (A) 2D view of the aortic arch. (B) Aortic arch view with color flow in the hematoma, confirming the presence of the pseudoaneurysm. (Color version of figure is available online.)
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(59%-83%) and less specific (63%-93%) than spiral CT in this setting, and the latter technique has been proposed as gold standard in case of suspected acute aortic syndrome.2,3 Indeed, in
atypical cases such as described here, echocardiography may be unable to establish the diagnosis unless there is a high index of suspicion for distal ascending aortic pathology.
REFERENCES 1. Chiu KW, Lakshminarayan R, Ettles DF: Acute aortic syndrome: CT findings. Clin Radiol 68:741-748, 2013 2. Sheikh AS, Ali K, Mazhar S: Acute Aortic Syndrome. Circulation 128:1122-1127, 2013
3. Hagan PG, Nienaber CA, Isselbacher EM, et al: The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA 283:897-903, 2000
