LETTERS TO THE EDITORe38

community on the management of the perioperative Takotsubocardiomyopathy (TTC).

However, after reading the letter from Yalcinkaya and co-workers,1 we would like to underscore some issues.

We focused exclusively on TTC associated with cardiogenicshock immediately after cardiac surgery. Due to this particularsetting, cardiac magnetic resonance imaging does not representa feasible diagnostic option.

Moreover, the authors conclude that “it is advised to be morecareful when IABP as well as inotropic agents are beingconsidered in TTC.” We do agree with the pathophysiologicrationale of this statement; but to date, we have had no otheroption to treat patients with TTC and cardiogenic shock.

As to the possibility that a compensatory reversible hyper-contractile basal wall could result in left ventricular outflowtract (LVOT) obstruction, we think that transthoracic echocar-diography (TTE), which is performed as the first-line diagnos-tic examination, could rule out the obstruction itself.

In a systematic review published in the European HeartJournal,2 a “transient, dynamic intraventricular pressure gradi-ent was found in 21 of 133 evaluated patients (15.8%, range:12.5-23%)” whereas the absence of hypertrophic cardio-myopathy represents one of the diagnostic criteria of TTC.

Moreover, hypercontractility alone may not be enough todetermine a significant LVOT obstruction,3 and, on thecontrary, a significant exercise-induced LVOT obstructioncan occur without hypertrophic obstructive cardiomyopathy,as seen in stress echocardiography in everyday clinical practice,especially in those patients with smaller LV end-diastolic andend-systolic diameters.3

Therefore, we disagree with the hypothetical statement thatIABP should not be used in smaller hearts in order to avoid apotentially harmful LVOT obstruction.

The treatment of perioperative TTC is still a matter ofdebate. The disease is underdiagnosed in the postoperativesetting and should be looked after with great attention inorder to enhance a straightforward pathophysiologicapproach 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 BelcolleViterbo, Italy

†Department of Cardiovascular ScienceS. Camillo-Forlanini Hospital, Rome, Italy

‡Department of Cardiomyopathies and Heart FailureBelcolle Hospital, Montefiascone Facility

Montefiascone (VT), Italy

REFERENCES

1. Yalcinkaya E, Celik M, Aribal S: Difficulty in management ofTakotsubo 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. EurHeart J 27:1523-1529, 2006

3. Zywica K, Jenni R, Pellikka PA, et al: Dynamic left ventricular outflowtract obstruction evoked by exercise echocardiography: Prevalence andpredictive 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 PatentForamen Ovale After Transurethral

Resection of Prostate:A Ticking Time Bomb

To the Editor:

The case of a 59-year-old woman with biatrial thrombusentrapped in a patent foramen ovale (PFO) and in cardiogenicshock who improved after an emergency surgical pulmonaryembolectomy has been published in this Journal.1 We report arelatively rare complication of pulmonary embolism (PE) andan impending paradoxical embolism due to a thrombus thatwas caught in transit in a PFO in the immediate postoperativeperiod in a patient who had an uneventful transurethralprostatectomy (TURP). Echocardiography and computed tomo-graphy helped in early detection that led to a successfulsurgical outcome.

A 72-year-old man with a history of hypertension anddiabetes mellitus underwent an elective TURP for benignprostatic hypertrophy under regional anesthesia. He wasambulatory within 12 hours. Preoperative hematologic profilewas normal except for thrombocytosis (platelets: 565,000/microliter). About 16 hours postoperatively, he developedsudden shortness of breath with bradycardia (o40 bpm),hypotension (systolic blood pressure o90 mmHg), and bloodoxygen desaturation that lasted for �30 minutes and wasmanaged with administration of oxygen and bolus doses ofatropine and epinephrine. A 12-lead electrocardiogram (ECG)after the initial resuscitation showed sinus tachycardia, rightventricular strain with incomplete RBBB, premature atrial beatswith deep S-wave in lead I, and inverted T-wave in lead III.Bedside transthoracic echocardiography revealed filamentousmasses in both atria attached to the interatrial septum slidingacross the tricuspid and mitral valves. Anticoagulation wasinitiated with low-molecular-weight heparin, and the patientwas referred to a tertiary care center for further management.

At that time, he was well-oriented and maintaining normalblood oxygen saturation on room air. There was no clinicalevidence of deep vein thrombosis in the limbs. Well’s criteriawas suggestive of a moderate-to-high clinical probability of PE(6 points). The patient’s hematologic investigations also weresuggestive of PE (troponin T-363 pg/mL [normal 0-14], B-typenatriuretic peptide [NTproBNP]- 3756 pg/mL [20-240], C-reactive protein [CRP]- 96, D-Dimer [cross linked d-dimerassay XDP]-10.6 [normal 0.1-0.5 mg/mL]). Computed tomo-graphy scan of the chest with contrast agent showed extensivepulmonary embolism involving the pulmonary trunk, main

Fig 2. Mid-esophageal short-axis view of the aortic valve demon-

strating right atrial thrombus entrapped in a patent foramen ovale.

LETTERS TO THE EDITOR e39

pulmonary arteries, segmental and sub-segmental arteries(Fig 1).

After an informed high-risk consent and induction of generalanesthesia, a TEE examination was performed. IntraoperativeTEE demonstrated a large thrombus extending from the inferiorvena cava into the right atrium and passing through the foramenof ovale into the left atrium (Fig 2). Emergency pulmonaryembolectomy with removal of the entrapped thrombus andclosure of PFO was performed with hypothermic cardiopulmon-ary bypass (CPB). The patient was separated from CPBuneventfully on milrinone infusion, 0.4 µg/kg/min. The patient’strachea was extubated after 6 hours of mechanical ventilation,and he was discharged home on the 10th postoperative day onmedication (oral carvidelol 6.25 mg BID, and warfarin 2 mgOD). He was followed up on the 28th postoperative day and wasfound to be in good health.

It is uncommon to find a trapped thrombus in a PFO,2 and itis very rare to diagnose an impending paradoxical embolism.3

In otherwise normal pulmonary vasculature, when there is aone-third or greater occlusion of the pulmonary artery, the rightatrial pressure exceeds the left atrial pressure.3 PE occurs in asmany as 85% to 94% of patients with paradoxical embolismwith ensuing pulmonary hypertension.3 The resultant pulmon-ary hypertension can lead to an acute elevation in the right-heart pressures that can open a foramen ovale, producing aright-to-left shunt and allow migration of a thrombus throughit.1

The term “venous thromboembolism” refers to deep venousthrombosis and/or pulmonary embolism.4 There is a 1.9%incidence of venous thromboembolism in patients undergoingopen urologic surgical procedures.4 Incidence of PE could bereduced to 0.45% in patients undergoing endoscopic proce-dures like TURP with usage of mechanical methods ofthromboprophylaxis.5 The Best Practice statement by theAmerican Urological Association is against specific prophy-laxis other than early mobilization in patients undergoingtransurethral surgery,6 justifying the fact that the patient in thiscase report was not on antithrombotic drugs.

As per the definition of a massive acute PE with associatedcriteria for outcome offered by Jaff and colleagues,7 our patient

Fig 1. Computed tomographic scan of the chest with contrast

agent demonstrating extensive pulmonary embolism involving the

pulmonary trunk and the main pulmonary arteries.

had a poor prognosis. By the timely detection and earlysurgical intervention, the patient had a successful outcome.

PE following TURP is rare. The incidence of PFO is quitehigh in the general population, and an impending paradoxicalembolism can occur after a massive PE in susceptible patientsdue to acute rise in the right heart chamber pressures. As animpending paradoxical embolism is associated with a highmortality rate (16-21%), it is important that this condition isdiagnosed at the earliest and corrective measures taken.8

Computed tomography scan and echocardiography are themainstay for diagnosis of this condition. In many cases, urgentcardiac surgical intervention is vital if at all possible if thepatient is to survive.

Madan Mohan Maddali, MDGopalakrishnan Nair Sanjeev, MD

Department of AnesthesiaRoyal Hospital

Muscat, Sultanate of Oman

REFERENCES

1. Alingrin J, Carillion A, Martin A, et al: Major pulmonary embolismand patent foramen ovale. J Cardiothorac Vasc Anesth 27:e30-e31, 20132. 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

RV

LV

RA LA

Fig 1. Four-chamber view. Right ventricle dilatation and signifi-

cant left ventricle compression. LA, left atrium; LV, left ventricle;

RA, right atrium; RV, right ventricle.

LETTERS TO THE EDITORe40

3. Shah DK, Ritter MJ, Sinak LJ, et al: Paradoxical embolus caughtin transit through a patent foramen ovale. J Card Surg 26:151-153, 20114. Rice KR, Brassell SA, McLeod DG: Venous thromboembolius in

urologic surgery: Prophylaxis, diagnosis, and treatment. Rev Urol 12:e111-e124, 20105. Donat R, Mancey-Jones B: Incidence of thromboembolism after

transurethral resection of the prostate (TURP)—a study on TED stockingprophylaxis and literature review. Scand J Urol Nephrol 36:119-123, 20026. Forrest JB, Clemens JQ, Finamore P, et al: AUA Best Practice

Statement for the prevention of deep vein thrombosis in patientsundergoing urologic surgery. J Urol 181:1170-1177, 20097. Jaff MR, McMurtry MS, Archer SL, et al: Management of

massive and submassive pulmonary embolism, iliofemoral deep veinthrombosis, and chronic thromboembolic pulmonary hypertension:A scientific statement from the American Heart Association. Circula-tion 123:1788-1830, 20118. Nemoto A, Kudo M, Yamabe K, et al: Successful surgical

treatment for a thrombus straddling a patent foramen ovale: A casereport. J Cardiothorac Surg 8:138, 2013

http://dx.doi.org/10.1053/j.jvca.2014.02.007

Focused Assessed TransthoracicEchocardiography for the Diagnosis ofFat Embolism in an Orthopedic Patient

With Hip Hemiarthroplasty

To the Editor:

In hip arthroplasty fat embolism can be caused by intrame-dullary manipulations during the placement of femoral compo-nents. Development and the passage of fat emboli into thevenous circulation and right cardiac chambers can result inobstruction of the pulmonary circulation, pulmonary hyperten-sion and hemodynamic instability.1

Focused Assessed Transthoracic Echocardiography (FATE)allows rapid, noninvasive, point-of-care assessment of ventri-cular function, valvular integrity volume status and fluidresponsiveness.2 In addition, transthoracic echocardiographycan facilitate the diagnosis and management of patients withcardiac emboli of any origin. 3–5 This rare case emphasizes therole of FATE in the diagnosis of fat embolism in an orthopedicpatient in the post anesthetic care unit (PACU).

An 83-year-old male patient was scheduled for left hiphemiarthroplasty. After spinal anesthesia with moderate seda-tion the surgical procedure was completed. Standard monitor-ing, including electrocardiography, pulse oximetry, andnoninvasive blood pressure monitoring was applied. Bloodpressure, oxygenation, and cardiac function monitoring showedthat all vital signs were in the normal range throughout theprocedure.

Approximately half an hour after his admission to the PACUthe patient showed bradyarrhythmia (35 bpm), hypotension (85/45 mmHg) and gradually worsening peripheral oxygen satura-tion 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 theright cardiac chambers (Video 1). The patient quickly becameunresponsive, 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 hemodynamicsupport were immediately accomplished. FATE was repeatedand showed a dilated hypokinetic right ventricle with the leftventricle significantly compressed (Fig. 1). Soon after, no heartrate response was noted and immediate cardiopulmonary resus-citation was started. Further images of the heart chambersconfirmed absence of contractility in both ventricles. Althoughmultiple resuscitation attempts were done, the outcome was fatal.

This case highlights that the availability of FATE allowedus to immediately diagnose the source of embolic materials andto conduct resuscitation in an orthopedic patient with hypoxiaand cardiovascular collapse.

APPENDIX A. SUPPORTING INFORMATION

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

Theodosios Saranteas, MD*

Georgia Kostopanagiotou, MD*

Fotios Panou, MD†

*Department of Anesthesia and Cardiovascular Care MedicalSchool, University of Athens, Attikon Hospital of Athens

†University of Athens, Second Cardiology DepartmentAttikon University Hospital of Athens

Haidari, Athens, Greece

REFERENCES

1. Hagley SR: The fulminant fat embolism syndrome. AnaesthIntensive Care 11:162-166, 19832. Cowie BS: Focused transthoracic echocardiograph in the perio-

perative period. Anaesth Intensive Care 38:823-836, 20103. Saranteas T, Kostopanagiotou G, Tzoufi M, et al: Incidence

of inferior vena cava thrombosis detected by transthoracic