community on the management of the perioperative Takotsubo cardiomyopathy (TTC). However, after reading the letter from Yalcinkaya and coworkers,1 we would like to underscore some issues. We focused exclusively on TTC associated with cardiogenic shock immediately after cardiac surgery. Due to this particular setting, cardiac magnetic resonance imaging does not represent a feasible diagnostic option. Moreover, the authors conclude that “it is advised to be more careful when IABP as well as inotropic agents are being considered in TTC.” We do agree with the pathophysiologic rationale of this statement; but to date, we have had no other option to treat patients with TTC and cardiogenic shock. As to the possibility that a compensatory reversible hypercontractile basal wall could result in left ventricular outflow tract (LVOT) obstruction, we think that transthoracic echocardiography (TTE), which is performed as the first-line diagnostic examination, could rule out the obstruction itself. In a systematic review published in the European Heart Journal,2 a “transient, dynamic intraventricular pressure gradient was found in 21 of 133 evaluated patients (15.8%, range: 12.5-23%)” whereas the absence of hypertrophic cardiomyopathy represents one of the diagnostic criteria of TTC. Moreover, hypercontractility alone may not be enough to determine a significant LVOT obstruction,3 and, on the contrary, a significant exercise-induced LVOT obstruction can occur without hypertrophic obstructive cardiomyopathy, as seen in stress echocardiography in everyday clinical practice, especially in those patients with smaller LV end-diastolic and end-systolic diameters.3 Therefore, we disagree with the hypothetical statement that IABP should not be used in smaller hearts in order to avoid a potentially harmful LVOT obstruction. The treatment of perioperative TTC is still a matter of debate. The disease is underdiagnosed in the postoperative setting and should be looked after with great attention in order to enhance a straightforward pathophysiologic approach to this disease. Let us put out the fire. Giordano Zampi, MD* Amedeo Pergolini, MD† Daniele Pontillo, MD‡ Francesco Musumeci, MD† Giovanni Casili, MD† *U.O.C. Cardiologia ed Emodinamica Ospedale Belcolle Viterbo, Italy †Department of Cardiovascular Science S. Camillo-Forlanini Hospital, Rome, Italy ‡Department of Cardiomyopathies and Heart Failure Belcolle Hospital, Montefiascone Facility Montefiascone (VT), Italy REFERENCES 1. Yalcinkaya E, Celik M, Aribal S: Difficulty in management of Takotsubo cardiomyopathy. J Cardiothorac Vasc Anesth [In press] 2. Gianni M, Dentali F, Grandi AM, et al: Apical ballooning syndrome or Takotsubo cardiomyopathy: A systematic review. Eur Heart J 27:1523-1529, 2006

3. Zywica K, Jenni R, Pellikka PA, et al: Dynamic left ventricular outflow tract obstruction evoked by exercise echocardiography: Prevalence and predictive factors in a prospective study. Eur J Echocardiogr 9:665-671, 2008 http://dx.doi.org/10.1053/j.jvca.2014.02.004

Entrapped Thrombus in a Patent Foramen Ovale After Transurethral Resection of Prostate: A Ticking Time Bomb To the Editor: The case of a 59-year-old woman with biatrial thrombus entrapped in a patent foramen ovale (PFO) and in cardiogenic shock who improved after an emergency surgical pulmonary embolectomy has been published in this Journal.1 We report a relatively rare complication of pulmonary embolism (PE) and an impending paradoxical embolism due to a thrombus that was caught in transit in a PFO in the immediate postoperative period in a patient who had an uneventful transurethral prostatectomy (TURP). Echocardiography and computed tomography helped in early detection that led to a successful surgical outcome. A 72-year-old man with a history of hypertension and diabetes mellitus underwent an elective TURP for benign prostatic hypertrophy under regional anesthesia. He was ambulatory within 12 hours. Preoperative hematologic profile was normal except for thrombocytosis (platelets: 565,000/ microliter). About 16 hours postoperatively, he developed sudden shortness of breath with bradycardia (o40 bpm), hypotension (systolic blood pressure o90 mmHg), and blood oxygen desaturation that lasted for 30 minutes and was managed with administration of oxygen and bolus doses of atropine and epinephrine. A 12-lead electrocardiogram (ECG) after the initial resuscitation showed sinus tachycardia, right ventricular strain with incomplete RBBB, premature atrial beats with deep S-wave in lead I, and inverted T-wave in lead III. Bedside transthoracic echocardiography revealed filamentous masses in both atria attached to the interatrial septum sliding across the tricuspid and mitral valves. Anticoagulation was initiated with low-molecular-weight heparin, and the patient was referred to a tertiary care center for further management. At that time, he was well-oriented and maintaining normal blood oxygen saturation on room air. There was no clinical evidence of deep vein thrombosis in the limbs. Well’s criteria was suggestive of a moderate-to-high clinical probability of PE (6 points). The patient’s hematologic investigations also were suggestive of PE (troponin T-363 pg/mL [normal 0-14], B-type natriuretic peptide [NTproBNP]- 3756 pg/mL [20-240], Creactive protein [CRP]- 96, D-Dimer [cross linked d-dimer assay XDP]-10.6 [normal 0.1-0.5 mg/mL]). Computed tomography scan of the chest with contrast agent showed extensive pulmonary embolism involving the pulmonary trunk, main


pulmonary arteries, segmental and sub-segmental arteries (Fig 1). After an informed high-risk consent and induction of general anesthesia, a TEE examination was performed. Intraoperative TEE demonstrated a large thrombus extending from the inferior vena cava into the right atrium and passing through the foramen of ovale into the left atrium (Fig 2). Emergency pulmonary embolectomy with removal of the entrapped thrombus and closure of PFO was performed with hypothermic cardiopulmonary bypass (CPB). The patient was separated from CPB uneventfully on milrinone infusion, 0.4 µg/kg/min. The patient’s trachea was extubated after 6 hours of mechanical ventilation, and he was discharged home on the 10th postoperative day on medication (oral carvidelol 6.25 mg BID, and warfarin 2 mg OD). He was followed up on the 28th postoperative day and was found to be in good health. It is uncommon to find a trapped thrombus in a PFO,2 and it is very rare to diagnose an impending paradoxical embolism.3 In otherwise normal pulmonary vasculature, when there is a one-third or greater occlusion of the pulmonary artery, the right atrial pressure exceeds the left atrial pressure.3 PE occurs in as many as 85% to 94% of patients with paradoxical embolism with ensuing pulmonary hypertension.3 The resultant pulmonary hypertension can lead to an acute elevation in the rightheart pressures that can open a foramen ovale, producing a right-to-left shunt and allow migration of a thrombus through it.1 The term “venous thromboembolism” refers to deep venous thrombosis and/or pulmonary embolism.4 There is a 1.9% incidence of venous thromboembolism in patients undergoing open urologic surgical procedures.4 Incidence of PE could be reduced to 0.45% in patients undergoing endoscopic procedures like TURP with usage of mechanical methods of thromboprophylaxis.5 The Best Practice statement by the American Urological Association is against specific prophylaxis other than early mobilization in patients undergoing transurethral surgery,6 justifying the fact that the patient in this case report was not on antithrombotic drugs. As per the definition of a massive acute PE with associated criteria for outcome offered by Jaff and colleagues,7 our patient


Fig 2. Mid-esophageal short-axis view of the aortic valve demonstrating right atrial thrombus entrapped in a patent foramen ovale.

had a poor prognosis. By the timely detection and early surgical intervention, the patient had a successful outcome. PE following TURP is rare. The incidence of PFO is quite high in the general population, and an impending paradoxical embolism can occur after a massive PE in susceptible patients due to acute rise in the right heart chamber pressures. As an impending paradoxical embolism is associated with a high mortality rate (16-21%), it is important that this condition is diagnosed at the earliest and corrective measures taken.8 Computed tomography scan and echocardiography are the mainstay for diagnosis of this condition. In many cases, urgent cardiac surgical intervention is vital if at all possible if the patient is to survive. Madan Mohan Maddali, MD Gopalakrishnan Nair Sanjeev, MD Department of Anesthesia Royal Hospital Muscat, Sultanate of Oman


Fig 1. Computed tomographic scan of the chest with contrast agent demonstrating extensive pulmonary embolism involving the pulmonary trunk and the main pulmonary arteries.

1. Alingrin J, Carillion A, Martin A, et al: Major pulmonary embolism and patent foramen ovale. J Cardiothorac Vasc Anesth 27:e30-e31, 2013 2. Acikel S, Ertem AG, Kiziltepe U, et al: Double-edged sword in the heart: Trapped deep venous thrombus in a patent foramen ovale. Blood Coagul Fibrinolysis 23:673-675, 2012



3. Shah DK, Ritter MJ, Sinak LJ, et al: Paradoxical embolus caught in transit through a patent foramen ovale. J Card Surg 26:151-153, 2011 4. Rice KR, Brassell SA, McLeod DG: Venous thromboembolius in urologic surgery: Prophylaxis, diagnosis, and treatment. Rev Urol 12: e111-e124, 2010 5. Donat R, Mancey-Jones B: Incidence of thromboembolism after transurethral resection of the prostate (TURP)—a study on TED stocking prophylaxis and literature review. Scand J Urol Nephrol 36:119-123, 2002 6. Forrest JB, Clemens JQ, Finamore P, et al: AUA Best Practice Statement for the prevention of deep vein thrombosis in patients undergoing urologic surgery. J Urol 181:1170-1177, 2009 7. Jaff MR, McMurtry MS, Archer SL, et al: Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: A scientific statement from the American Heart Association. Circulation 123:1788-1830, 2011 8. Nemoto A, Kudo M, Yamabe K, et al: Successful surgical treatment for a thrombus straddling a patent foramen ovale: A case report. J Cardiothorac Surg 8:138, 2013




Fig 1. Four-chamber view. Right ventricle dilatation and significant left ventricle compression. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.


Focused Assessed Transthoracic Echocardiography for the Diagnosis of Fat Embolism in an Orthopedic Patient With Hip Hemiarthroplasty To the Editor: In hip arthroplasty fat embolism can be caused by intramedullary manipulations during the placement of femoral components. Development and the passage of fat emboli into the venous circulation and right cardiac chambers can result in obstruction of the pulmonary circulation, pulmonary hypertension and hemodynamic instability.1 Focused Assessed Transthoracic Echocardiography (FATE) allows rapid, noninvasive, point-of-care assessment of ventricular function, valvular integrity volume status and fluid responsiveness.2 In addition, transthoracic echocardiography can facilitate the diagnosis and management of patients with cardiac emboli of any origin. 3–5 This rare case emphasizes the role of FATE in the diagnosis of fat embolism in an orthopedic patient in the post anesthetic care unit (PACU). An 83-year-old male patient was scheduled for left hip hemiarthroplasty. After spinal anesthesia with moderate sedation the surgical procedure was completed. Standard monitoring, including electrocardiography, pulse oximetry, and noninvasive blood pressure monitoring was applied. Blood pressure, oxygenation, and cardiac function monitoring showed that all vital signs were in the normal range throughout the procedure. Approximately half an hour after his admission to the PACU the patient showed bradyarrhythmia (35 bpm), hypotension (85/ 45 mmHg) and gradually worsening peripheral oxygen saturation levels. FATE, performed by a competent anesthesiologist, revealed inferior vena cava dilatation (2.2 cm), with hyperechoic

multiple emboli passing through the inferior vena cava in the right cardiac chambers (Video 1). The patient quickly became unresponsive, his peripheral blood pressure decreased to 70/ 35 mmHg and arterial blood gas revealed PO2 ¼ 55 mmHg (PO2/FiO2 ¼ 110). Subsequently, intubation and hemodynamic support were immediately accomplished. FATE was repeated and showed a dilated hypokinetic right ventricle with the left ventricle significantly compressed (Fig. 1). Soon after, no heart rate response was noted and immediate cardiopulmonary resuscitation was started. Further images of the heart chambers confirmed absence of contractility in both ventricles. Although multiple resuscitation attempts were done, the outcome was fatal. This case highlights that the availability of FATE allowed us to immediately diagnose the source of embolic materials and to conduct resuscitation in an orthopedic patient with hypoxia and cardiovascular collapse. APPENDIX A. SUPPORTING INFORMATION

Supplementary material cited in this article is available online at doi:10.1053/j.jvca.2014.03.001.

Theodosios Saranteas, MD* Georgia Kostopanagiotou, MD* Fotios Panou, MD† *Department of Anesthesia and Cardiovascular Care Medical School, University of Athens, Attikon Hospital of Athens †University of Athens, Second Cardiology Department Attikon University Hospital of Athens Haidari, Athens, Greece REFERENCES 1. Hagley SR: The fulminant fat embolism syndrome. Anaesth Intensive Care 11:162-166, 1983 2. Cowie BS: Focused transthoracic echocardiograph in the perioperative period. Anaesth Intensive Care 38:823-836, 2010 3. Saranteas T, Kostopanagiotou G, Tzoufi M, et al: Incidence of inferior vena cava thrombosis detected by transthoracic

Entrapped thrombus in a patent foramen ovale after transurethral resection of prostate: a ticking time bomb.

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