Patent Foramen Ovale and Intracardiac Thrombus Identified by Transesophageal Echocardiography During Liver Transplantation

Patent Foramen Ovale and Intracardiac Thrombus Identified by Transesophageal Echocardiography During Liver Transplantation Enver Yerlioglu, MD, Vijay Krishnamoorthy, MD, Hoonbae Jeon, MD, FACS, Allen Gustin, MD, FCCP, and Ramona Nicolau-Raducu, MD, PhD

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ATENT FORAMEN OVALE (PFO) treatment is controversial in the general population because of the lack of randomized, prospective clinical trials, making the decision for PFO closure more difficult in high-risk patients such as those undergoing liver transplantation. CASE PRESENTATION

A 64-year-old man with a body mass index of 33.4 kg/m2, end-stage liver disease secondary to alcohol and hepatocellular carcinoma, and a Model for End-Stage Liver Disease score of 28 who presented for orthotopic liver transplantation (OLT) is described. His past medical history was significant for pancreaticoduodenectomy for a benign pancreatic tumor and a PFO with an interatrial septal aneurysm, which was revealed by a preoperative pretransplant transesophageal echocardiogram (TEE). His vital signs included a temperature of 98°F, blood pressure (BP) of 140/73 mmHg, heart rate (HR) of 87 beats/ min, and oxygen saturation (SaO2) of 100% on room air. His preoperative coagulation variables showed a hemoglobin of 12.1 g/dL (normal range, 13.2-18 g/dL); a platelet (PLT) count of 46 ⫻ 103/mm3 (normal range, 200-300 ⫻ 103/mm3); and a prothrombin time (PT) of 17.3 seconds (normal range, 11.5-15 seconds), an international normalized ratio (INR) of 1.39 (normal range, ⬍1), and an activated thromboplastin time (PTT) of 37 seconds (normal range, 26-36 seconds). After general anesthesia was induced, invasive catheters were placed using TEE guidance (Philips iE33a1 for monitoring and resuscitation, Philips Healthcare, Bothell, WA). These catheters included the following: an 18F venovenous bypass cannula, a 9F double-lumen pulmonary artery introducer catheter, and a 20-G arterial catheter. The following cardiac parameters were recorded continuously throughout the procedure: cardiac index (CI), venous oxygen saturation (SvO2), central venous pressure (CVP), and systolic/diastolic pulmonary artery pressure (PAP). An intraoperative baseline TEE revealed normal left and right ventricular function, normal valvular structures, a PFO on color-flow Doppler with a left-to-right shunt and a width of 0.8 cm (Fig 1), an atrial septal aneurysm, and a prominent Eustachio valve (Video 1 [supplementary videos are available online]). The patient tolerated the preanhepatic (stage I, dissection phase) and the anhepatic phases (stage II, resection of cirrhotic liver) well and required minimal transfusion through these 2 stages: 4 U of packed red blood cells (PRBCs) and 4 U of fresh frozen plasma to keep hemoglobin above 8 g/dL and stable hemodynamic parameters. As the case progressed from stage I to II, the PLT count remained stable at 60 ⫻ 103/mm3, the INR increased to 2, and the fibrinogen (Fb) value decreased from 189 to 151 mg/dL but remained within normal limits (Fb, 150-400 mg/dL). At the beginning of stage II, both methylprednisolone, 500 mg, and basiliximab, 20 mg, were infused into the patient. End-to-side inferior venacaval anastomosis was completed, and the liver allograft was flushed with 500 mL of cold 5% albumin. The serum potassium value was 4.2

mEq/L (goal ⬍4.0 mEq/L). Given that the potassium was greater than 4.0, a portal venous blood flush also was performed in order to help prevent the severe hyperkalemia that can occur with liver revascularization.2 Vascular anastomosis was completed, and the vascular crossclamps were removed to establish hepatic reperfusion (stage III) after only 24 minutes of warm ischemia time and 261 minutes of cold ischemia time. Reperfusion during the first minute was tolerated well, with a BP of 110/60 mmHg, HR of 110 beats/min, SaO2 of 100% on 100% FIO2, systolic/diastolic PAP of 30/18 mmHg, CVP of 10 mmHg, CI of 5.5 L/min/m2, and SvO2 of 81%. Five minutes after reperfusion, the patient’s BP suddenly decreased to 81/42 mmHg with an associated HR of 58 beats/min. A TEE revealed a large free-floating thrombus in the right atrium. The thrombus started in the inferior vena cava (IVC) (Video 2), extended into the PFO (Video 3), and was partially obstructing the tricuspid valve and right ventricular inflow (Video 4). The thrombus position was highly concerning given that a massive embolus could occur. If the thrombus further migrated into the left atrium through the PFO (Fig 2), then the potential of a systemic embolus existed. If the thrombus migrated into the right ventricle, then the potential of a massive pulmonary embolus existed. The surgeon was notified, and suction of the venous anastomosis site was initiated in order to decrease the right atrial pressure. The BP was increased with intravenous epinephrine, 50 ␮g, in order to increase the left atrial pressure, with the aim to keep a left-toright shunt through the PFO and maintain the thrombus in the right atrium. During this time, unfractionated heparin (2,000 U ⫻ 2 boluses) was given at 5-minute intervals in order to stabilize the clot formation, which resulted in rapid resolution of the clot from the right ventricle inflow only 10 minutes after clot detection. No clinical signs of pulmonary embolism were noted because PAPs remained within normal limits with no right ventricular dysfunction and no wall motion abnormality on TEE. After the acute event, the patient became clinically coagulopathic (even though only a small dose of heparin was administrated) with oozing from the surgical site and surgical wound edges. The following laboratory values were found at this time: a PLT count of 51 ⫻ 103/mm3, hemoglobin of 8.5 g/dL, PT ⬎120 seconds, PTT ⬎300 seconds, and Fb ⬍100 mg/dL. From the University of Illinois at Chicago Medical Center, Chicago, IL. Address reprint requests to Ramona Nicolau-Raducu, MD, PhD, Department of Anesthesiology, University of Illinois at Chicago Medical Center, 1740 West Taylor Street, Suite 3200W, Chicago, IL 606127232. E-mail: [email protected] © 2012 Elsevier Inc. All rights reserved. 1053-0770/2606-0018$36.00/0 doi:10.1053/j.jvca.2011.05.003 Key words: patent foramen ovale, thrombus, transesophageal echocardiography, liver transplantation

Journal of Cardiothoracic and Vascular Anesthesia, Vol 26, No 6 (December), 2012: pp 1069-1073

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Fig 1.

YERLIOGLU ET AL

The midesophageal bicaval view of color Doppler flow showing a functional PFO.

These laboratory values were treated with the following blood products throughout the remaining time of the surgery: 12 U of PRBCs, 15 U of FFP, 2 U of platelet concentrate (6 pool each), and 10 U of cryoprecipitate. In addition, an epinephrine infusion (0.05 ␮g/kg/min) was initiated in order to maintain a mean arterial pressure above 65 mmHg. The hepatic artery and bile duct reconstructions were completed without any further events. The patient tolerated closure of the abdominal wall without issues and was transferred to the intensive care unit (ICU) without any further hemodynamic events. At the time of transfer from the operating room to the ICU, the hemoglobin was 9.0 mg/dL, the platelet count was 91 ⫻ 103/mm3, PT was 20.7 seconds, INR was 1.75, PTT was 35.6 seconds, and Fb was 203 mg/dL. The postoperative course was complicated by hemodynamic instability for the first 48 hours, which required further support with more blood products and increased epinephrine requirements. A troponin leak was identified postoperatively but was associated with no wall motion abnormalities by TEE or any associated electrocardiographic changes. The patient remained sedated for the first 48 hours while he stabilized hemodynamically. After the first 48 hours in the ICU, the sedation was

ceased, and the patient was slow to awaken. During this time of no sedation, no obvious neurologic deficit or body posturing was noted. A computed tomography (CT) scan of the head was obtained (now 72 hours after the transplant), which showed a left cerebellar hemorrhage (3/2 cm layering over cerebellar hemisphere). At the time of the CT scan of the head, the PLT count was 19 ⫻ 103/mm3 with an INR of 1.5. This coagulopathy was treated with a goal of a PLT count above 70 ⫻ 103/mm3 and an INR ⬍1.3. No neurologic intervention was necessary because serial CT scans of the head revealed no progression of the intracerebellar hemorrhage. An electroencephalogram did not show any epileptiform activity. Neurologically, the patient improved slowly without any motor deficit by postoperative day 5 and eventually was able to be extubated. Because the patient’s neurologic status improved so quickly, magnetic resonance imaging of the head was never performed in order to evaluate an ischemic etiology for cerebellar hemorrhage or other clinically insignificant ischemic issues of the cerebral cortex. Two weeks later, the patient was transferred to the rehabilitation service, was later discharged to home, and has been reported to be doing well. DISCUSSION

Fig 2. The midesophageal right ventricular inflow/outflow view of the clot migrating to the PFO. LA, left atrium; RA, right atrium; TH, intracardiac thrombus; EV, prominent eustachian valve.

An intracardiac thrombus has been reported during OLT with an incidence between 1.2%3 and 6.25%.4 Reviewing the literature of 26 case reports, Lerner et al4 revealed that the thromboembolic events occurred with a slight predominance during reperfusion in 37% of the cases (30% of the cases occurred during preanhepatic and 33% during the anhepatic phase). Venovenous bypass and antifibrinolytics were used in 45% and 69% of the reported cases, respectively, with an associated 30% intraoperative mortality.4 Even during an IVCsparing piggy-back surgical technique, there still can be a compromise of the IVC flow that potentially leads to venous stasis below the clamp. This venous stasis could predispose to the formation of clot in the IVC that could embolize after removal of the clamp.4 Portal venous blood (used for flushing out the University of Wisconsin solution) has the advantage of being a physiologic fluid, thus removing the acidotic mesenteric venous blood, and perhaps may result in more stable

PFO AND INTRACARDIAC THROMBUS

hemodynamic parameters during the reperfusion period.5 There is always a delay between finishing the anastomosis and removal of the IVC clamp, which can contribute to clot formation in the hepatic veins, while there is stagnant blood in the liver during that period of time. Activation of the intrinsic coagulation system and decreased clearance of activated coagulation factors (during stage II) have been proposed as mechanisms for a hypercoagulable state that may lead to thrombotic events immediately after reperfusion.3 The authors think that this was one of the contributing factors in clot formation in this patient who already had a high risk of having a hypercoagulable state given his malignancy. This patient showed no obvious signs of coagulopathy and did not require significant use of blood products during stages I and II. In addition, the quality of the 54-year-old donor liver was considered good and not antifibrinolytic, and no venovenous bypass was used during this surgery. Regarding treatment of the free-floating intracardiac thrombus, many heroic measures have been described in the literature, with variable results. The measures include surgical embolectomy using cardiopulmonary bypass, venovenous oxygenation with systemic or local thrombolytics, heparin anticoagulation, and interventional suction catheter devices.6-8 No matter which approach of thrombus removal is chosen, resuscitative efforts should begin immediately in the case of an intracardiac thrombus including inotropes, vasopressors, and fluid/volume therapy. Direct suctioning of the IVC has been proposed as a means to evacuate the intracardiac thrombus and has been used successfully in previous studies at preventing a right atrial thrombus from migrating into the pulmonary artery.9 The administration of heparin was beneficial in the present case in preventing further clot formation while allowing/accelerating the patient’s endogenous fibrinolytic pathways to proceed.3,4,9 A PFO is a well-recognized risk factor for ischemic strokes. The prevalence of a PFO in the general population is ⬎25%10, and it is higher among stroke patients by more than 30%.11,12 Besides case reports regarding paradoxic embolism, which does occur during liver transplantation,13,14 only 1 retrospective PFO study focusing on liver transplant patients exists. From that study, Alba et al15 concluded that a PFO does not appear to affect patient outcomes during the perioperative period after liver transplantation as far as the duration of mechanical ventilation, dialysis, and the incidence of delirium, stroke, or 30-day mortality rate.15 The limitations of the study included the small sample size (27 patients), no quantification of the PFO size, and also none of the patients developed pulmonary emboli perioperatively. Transesophageal echocardiography is the “gold standard” in diagnosing any PFO, but transcranial Doppler showed a specificity of 75% to 100% and a sensitivity of 69% to 91% compared with TEE depending on the technique used.16 Thus, transcranial Doppler can be used as an alternative tool for diagnosis in patients in whom there is a TEE contraindication. This patient had a PFO diagnosed preoperatively (an atrial septal aneurysm was identified and a right-to-left shunt was noted, but no further measurements were provided), yet it was not categorized as being significant during the cardiac risk stratification. Cardiology did not include any further recommendations for the management of this patient based on the

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information provided. Ultimately, the intraoperative TEE examination identified a large PFO before the identification of the right atrial thrombus. Watching in real-time ultrasound how the thrombus was evolving and moving toward both the PFO and the right ventricle made the authors realize that the identification of a PFO can be a contributing factor for the multiple complications to which a liver transplant patient can be exposed. The reversal of flow through a PFO can happen at any time during liver transplantation with air, a free-floating clot, and/or debris passing into the left heart. All of these factors can lead to a possible cerebral or cardiac embolization. Three factors are important in determining the likelihood that a PFO will be of clinical significance: its size, the pressure gradient between the right atrium and the left atrium, and the direction of IVC flow.17 Many studies show that the combination of a PFO and an atrial septal aneurysm confers a 3- to 5-fold increased risk for recurrent events compared with patients with a PFO alone.18-20 The motion of the fossa ovalis membrane may promote paradoxic shunting through mechanical action by enhancing the preferential orientation of the flow from the IVC toward the foramen ovale; it may also increase the PFO diameter because of the highly mobile atrial septal tissue, especially in stress situations.21 A PFO diameter greater than 4 mm has been identified as a high risk of recurrent strokes in a study by Schuchlenz et al.22 In the study by Konstantinides et al,23 the detection of a PFO was an important predictor of death and an adverse outcome (ischemic stroke and peripheral arterial embolism) in patients with major pulmonary embolism, with an overall risk of a complicated in-hospital course of 5.2 times higher in the PFO group. The reported clinical incidence of cerebrovascular complications was 1.7% to 6.5% and 32.7% in postmortem patients after OLT both worldwide and in the United States, respectively.24 After OLT, the mortality rate of cerebrovascular complications or intracranial hemorrhage was 57% to 100%.24 Regarding the intracerebellar hemorrhage diagnosed postoperatively in the present patient, the authors could not exclude an ischemic etiology for cerebellar hemorrhage. The authors also could not exclude that the hypotension and troponin leak were not related to a paradoxic embolism; the cardiology department believed they were related to demand ischemia. Because of the high mortality rate that occurs once the cerebrovascular complication is identified, PFO screening appears useful for the preoperative evaluation of liver transplant candidates, and perhaps a more aggressive intervention is necessary. The authors noticed a lack of intervention from the cardiologist whenever a PFO was identified in a liver transplant candidate during preoperative evaluation. This is becoming more important in centers that are performing high-risk transplants where more coagulation disturbances, hypotension, and/or more severe reperfusion syndromes are expected, making the risk of paradoxic embolism much higher in the perioperative period. Based on current literature regarding PFOs,17,25-28 the authors propose a protocol that they are trying to implement in their center on liver transplant candidates for PFO screening and quantification of the size of the shunt with possible percutaneous device closure before the transplant if the shunt is signif-

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YERLIOGLU ET AL

Transthoracic echocardiography screening, Color Doppler Flow, followed by bubble study

Bubble study positive /Valsalva maneuver/cough

Small shunt < 6 bubbles

Medium shunt 6-20 bubbles

Large shunt > 20 bubbles

Consider Transesophageal echocardiography (TEE) “Gold standard”

- Calculate Qp/Qs ratio* of the pulmonary flow (Qp) measured in the RV outflow tract (RVOT) and systemic flow (Qs) measured in the LV outflow tract (LVOT). - Assess RV size and function

Bubble study positive after 5 sec without Valsalva maneuver

Bubble study negative

Transpulmonary shunt

If absolute TEE contraindication**

Repeat the bubble study with - Transcranial Doppler (TCD)

> 20 signals on TCD +/- Presence of the following: -cryptogenic stroke -amnesia -migraine with an aura -platypnea-orthodeoxia syndrome -decompression sickness

- If Qp/Qs > 1.5 +/- RV dilatation - Atrial septum aneurysm - Chiari network - Prominent Eustachian valve - IVC flow direction

Right heart catheterization with pulmonary artery pressure and shunt evaluation

If no severe pulmonary hypertension, then Consider PFO closure before liver transplant

Fig 3. The PFO screening protocol for liver transplant candidates. *The cross-sectional area (CSA) and velocity time integral (VTI) are calculated at the right ventricle outflow tract (RVOT) and left ventricle outflow tract (LVOT) site. Qp ⴝ CSARVOT ⴛ VTIRVOT, Qs ⴝ CSALVOT ⴛ VTILVOT, and CSAⴝ [⌸(D/2)]2. D is the diameter. **Esophageal stricture, trachesophageal fistula, postesophageal surgery, and esophageal trauma.

icant (Fig 3). The choice of medical therapy with antiplatelet agents or vitamin K antagonists versus percutaneous device closure has been the subject of debate with a lack of randomized clinical trials because of poor referral for enrollment.29 Medical treatment is not a feasible option in liver transplant candidates because of the possible reversal of flow perioperatively when hypotension/reperfusion of the right heart can override the pressure of the left heart with shunt reversal via an open PFO. Primary surgical repair rarely is advocated in the current era and definitely should be avoided in a patient with liver failure because of the well-known high mortality rate associated with open cardiac procedure on Child score B or C liver patients. Within the last several years, momentum is gaining for the consideration of closing a PFO much earlier than previously thought. Given the ease of the percutaneous closure devices, the balance between the risks and benefits of PFO closure may appear to be shifting in favor of closure with a well-described technique performed in the interventional cardiology suite.28,30 Regarding complications associated with cardiac catheterization on liver patients, there are some studies indicating that cardiac catheterization can be performed safely in this patient population with the correction of coagulopathy and meticulous attention to the procedural technique.31,32

CONCLUSIONS

Liver transplantation is a high-risk procedure. Given this case report, the authors see the potential for further complications when patients presenting for liver transplantation have a PFO. The risk for paradoxic emboli through a PFO may be quite high in the perioperative period of liver transplantation. Given the various stages of liver transplant surgery, hemodynamic alterations with or without elevated intracardiac pressures may cause an insignificant PFO to become significant. Transesophageal echocardiography is the only method that can provide the constant monitoring for the formation of any intracardiac clots by direct visualization as well as being the gold standard for the identification of a PFO. In the authors’ opinion, all candidates for OLT should be assessed for PFO in their preoperative evaluation as part of cardiac risk stratification. If a PFO is found preoperatively and meets the criteria as outlined in Figure 3, then the authors recommend that the closure of the PFO be considered before liver transplantation. Also, it is the authors’ practice to use TEE for the intraoperative management of all patients without any absolute contraindication33 during liver transplantation.

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