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Anesthetic Management of a Patient With Dynamic Left Ventricular Outflow Tract Obstruction With Systolic Anterior Movement of the Mitral Valve Undergoing Redo–Orthotopic Liver Transplantation
CASE REPORTS
Anesthetic Management of a Patient With Dynamic Left Ventricular Outflow Tract Obstruction With Systolic Anterior Movement of the Mitral Valve Undergoing Redo–Orthotopic Liver Transplantation Debashis Roy, MD, and Fiona E. Ralley, MBChB, FRCA
E
ND-STAGE LIVER DISEASE is associated with significant hemodynamic changes.1,2 By the time patients present for liver transplantation, they often have a hyperdynamic circulation with a profound increase in their cardiac output (CO) and reduced systemic vascular resistance (SVR). This combination of hemodynamic derangements makes these patients especially prone to dynamic left ventricular outflow tract obstruction (DLVOTO). Aniskevich et al3 recently published a case report in which DVLOTO with systolic anterior motion (SAM) of the mitral valve was detected for the first time during the reperfusion phase of orthotopic liver transplantation (OLT) in a patient with an unremarkable preoperative cardiac evaluation and uneventful preanhepatic and anhepatic stages.3 A case of preoperative DLVOTO and SAM of the mitral valve with atrial fibrillation and significant hemodynamic instability presenting in a patient scheduled for redo-OLT is presented. The case was managed successfully with preoperative cardioversion to sinus rhythm and intraoperative hemodynamic management guided by transesophageal echocardiography (TEE). CASE REPORT The patient’s wife gave written consent to report this case. A 59-year-old man (108 kg, 177.5 cm) presented at the authors’ institution for redo-OLT. Fifteen years previously, he had undergone OLT for the treatment of cirrhosis secondary to hepatitis C virus and alcoholism. Over the previous 18 months, he had developed chronic rejection and was listed for redo-OLT. He had been scheduled to undergo redo-OLT, but at the last minute the organ was required by a more urgent recipient (in another province). However, because of his declining health, it was decided to keep the patient in the hospital for preoperative optimization. His past medical history was significant only for gout. Over the next few days, he developed
From the Department of Anesthesia and Perioperative Medicine, London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada. Address reprint requests to Fiona E. Ralley, MBChB, FRCA, Department of Anesthesia and Perioperative Medicine, LHSC University Hospital, Room C3-110, 339 Windermere Road, London, ON, Canada N6A 5A5. E-mail: [email protected] © 2012 Elsevier Inc. All rights reserved. 1053-0770/2602-0017$36.00/0 doi:10.1053/j.jvca.2011.02.014 Key words: liver transplantation, dynamic left ventricular outflow tract obstruction, systolic anterior motion of the mitral valve, transesophageal echocardiography 274
massive ascites, causing significant shortness of breath at rest. During the subsequent paracentesis, the patient became profoundly hypotensive. This was managed initially unsuccessfully with fluid resuscitation with albumin and a dopamine infusion for 2 to 3 days. Therefore, to rule out any cardiac abnormalities, transthoracic echocardiography was performed, which showed a hyperdynamic left ventricle with an ejection fraction of 80% and complete cavity obliteration during systole, left ventricular outflow tract obstruction with mean pressure gradient of 30 to 40 mmHg associated with severe SAM of the mitral valve, and moderate mitral regurgitation (Fig 1). The right side of the heart was normal. After extensive discussion among the anesthesiologists, the cardiologists, the transplant surgeons, and the patient’s family, it was decided that although it was high risk, redo-OLT was the only long-term option for this patient because the cardiac changes were dynamic with no intracardiac structural abnormalities. During the following 2 weeks while waiting for another suitable organ, the patient became more unstable. He developed hepatorenal syndrome with complete anuria and an increase in urea to 28.4 mmol/mL (80.39 mg/dL) and in creatinine to 403 mmol/mL (5.28 mg/dL). Because hemodialysis caused profound hypotension, he was started on continuous renal replacement therapy (PRISMA; Gambro Inc, Toronto, ON, Canada) 4 days before his subsequent transplant. At the same time, he developed hepatic encephalopathy secondary to a gastrointestinal bleed requiring transfer to the intensive care unit (ICU). His DVOTO was managed by an infusion of vasopressin (2.4 U/h) and by increasing his preload. Two days before his transplant, he developed atrial fibrillation, which was managed initially medically by maintaining his heart rate ⬍100 beats/min. Cardioversion was not considered at this time because it was felt unlikely to be successful or that the patient would not remain in sinus rhythm for any length of time. Furthermore, this would require that the patient be intubated before cardioversion because of his reduced conscious state and extubation would probably fail at that time. Immediately before transfer to the operating room for redo-OLT, he was intubated to protect his airway, cardioverted into sinus rhythm using 75 J, and started on amiodarone (a 150-mg bolus followed by an infusion of 1 mg/min) to try to maintain sinus rhythm. The preoperative laboratory testing showed a hemoglobin level of 83 mmol/mL, an international normalized ratio of 2.9, partial thromboplastin time of 67, and a platelet count of 26,000⫻109/L. After the induction of anesthesia with sufentanil, midazolam, and rocuronium, a left radial arterial catheter and the left internal jugular vein with a pulmonary catheter (right internal jugular vein was cannulated previously for dialysis) were inserted. Before surgical incision, the standard dose of 4.8 mg of recombinant activated factor VII (NovoSeven; Novo Nordisk Canada Inc, Mississauga, ON, Canada) was administered to try to reduce the bleeding during the prehepatic stage. The repeat international normalized ratio and partial thromboplastin time were 1.2 and 53, respectively.
Journal of Cardiothoracic and Vascular Anesthesia, Vol 26, No 2 (April), 2012: pp 274-276
DLVOTO IN REDO-OLT
275
Fig 1. Transthoracic echocardiography (parasternal long-axis view) showing the left ventricle during systole (complete obliteration of cavity) and SAM of the anterior mitral leaflet. LV, left ventricle; LA, left atrium; AO, aorta; MV, mitral valve; AV, aortic valve; AML, anterior mitral leaflet.
A transesophageal echocardiographic probe was inserted to monitor the cardiac function and to guide fluid administration. Table 1 describes the intraoperative problems, how they were managed, and the hemodynamic parameters. During the postreperfusion phase, the norepinephrine infusion was tapered slowly and discontinued, the vasopressin dose was reduced back to 2.4 U/h, and the phenylephrine dose was reduced to 40 g/min. The total operating time was 13 hours 40 minutes, with an estimated blood loss of ⬎20 L for which he received 42 U of packed red cells, 20 U of fresh frozen plasma, 10 U of platelets, 8 L of crystalloid, 1.5 L of colloid (Voluven; Fresenius Kabi Canada, Mississauga, ON, Canada), and 1 L of 5% albumin. After completion of surgery, the abdomen was packed open, and the patient was transferred to the ICU on vasopressin, 2.4 U/h, and phenylephrine, 40,g/min. Hemodynamic parameters at this time showed a heart rate of 88 beat/min, blood pressure of 102/56 mmHg, pulmonary arterial pressure of 39/21 mmHg, and a cardiac index of 7.4 L/m2/min. On the 3rd postoperative day (POD), with a well-functioning graft, the patient was returned to the operating room for removal of his
Fig 2. Transthoracic echocardiography (parasternal long-axis view) showing the left ventricle during systole and no SAM. LV, left ventricle; LA, left atrium; AO, aorta; MV, mitral valve; AV, aortic valve.
abdominal packs and formal wound closure. By POD 5, all vasopressor support had been discontinued, and on POD 9 repeat echocardiography showed no SAM, with normal left ventricular function and size, an ejection fraction of 67%, mild left atrial dilatation (4.9 cm), and a mildly dilated right ventricle (Fig 2). The patient was extubated on POD 14, and on POD 17 he was discharged from the ICU to the transplant unit. Renal function started to improve postoperatively, and by POD 45 dialysis was stopped. He was discharged home on POD 56. Unfortunately, after initially continuing to improve, his health gradually declined, and he died 16 months after his transplant. DISCUSSION
End-stage liver disease is associated with a hyperdynamic circulation leading to a profound increase in CO and a decrease in SVR.1,2 If there is a decrease in preload (eg, during bleeding, paracentesis, or cross-clamping of the inferior vena cava) or tachycardia (eg, during stress or reperfusion), then DLVOTO with SAM may be precipitated. In addition, during the reper-
Table 1. Intraoperative Problems, Management, and Outcomes Preanhepatic
Anhepatic (IVC XC ⫽ 67 min)
Reperfusion
Problems
DLVOTO with SAM secondary to massive blood loss from previous adhesions, portal hypertension, and coagulopathy
DLVOTO with SAM secondary to a decrease in venous return leading to a fall in preload
Management (titrated to maintain MBP ⬎70 mmHg and HR ⬍90 beats/min)
Phenylephrine (20-50 g/min) Amiodarone (1 mg/min) Esmolol (20-mg bolus) Massive blood transfusion Vasopressin infusion (4-8 U/h)
In addition to 1-5 of prehepatic norepinephrine (5-8 g/h)
DLVOTO with SAM secondary to release of toxin, interleukins, and complement factors from the donor’s liver and patient’s lower body Phenylephrine (up to max of 80 g/min) Amiodarone (1 mg/min) Vasopressin (up to max of 10 U/h) Norepinephrine (8 g/h)
Hemodynamics Heart rate (beats/min) IBP (mmHg) PAP (mmHg) CI (L/min/m2)
70-90 S 85-105 D 40-54 42/21-54/27 4.6-5.2
80-95 S 85-95 D 36-48 37/14-37/21 1.7-2.0
80-95 S 80-95 D 40-54 58/29 7.9
Abbreviations: IVC XC, inferior vena cava cross-clamp; HR, heart rate; IBP, invasive blood pressure; S, systolic; D, diastolic; MBP, mean blood pressure; PAP, pulmonary arterial pressure; CI, cardiac index.
276
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fusion stage of OLT, SVR may further be reduced, possibly also precipitating DLVOTO and SAM.3 The authors could find only 1 previous case report of DLVOTO without hypertrophy of the cardiac musculature.3 Aniskevich et al3 described a case in which they diagnosed DLVOTO by TEE during the reperfusion phase to assist in the diagnosis and management of refractory hypotension. Preoperative stress echocardiography and intraoperative preanhepatic and anhepatic phases had been unremarkable in this patient, and the authors postulated that the “loss of preload, coupled with the sudden drop in SVR, may have been enough to allow for a “perfect storm” in which a patient with a predisposition for DLVOTO may actually develop the obstruction.”3 Cywinski et al4 described a case in which DLVOTO was observed during preoperative stress echocardiography with normal hemodynamics. However, this patient had left ventricular hypertrophy with septal hypertrophy and only developed mild hemodynamic instability during the reperfusion stage, which was managed with low-dose vasopressor support. This case report differs from these previous case reports because the present patient developed preoperative DLVOTO with SAM without any obvious precipitating stress. Preoperatively, he was hemodynamically unstable requiring vasopressor support. At present, there are no clear guidelines for the management of these patients requiring OLT. Therefore, before the start of the case, the authors established 4 goals. The 1st goal was to maintain preload, especially during the dissection phase, when there was likely to be profound blood loss secondary to the adhesion from his previous OLT, his significant portal hypertension, and the concurrent coagulopathy. The rapid replacement of blood products was achieved with the use of a level 1 rapid infusion system (SIMS Level 1 Inc, Rockland, MA) and was guided by TEE and/or pulmonary arterial pressure. The 2nd goal was to maintain afterload by preventing any reduction in the SVR using phenylephrine, vasopressin, and norepinephrine. The 3rd goal was to avoid tachycardia, for which esmolol boluses were used to maintain a heart rate ⬍90 beats/min. The
4th goal was to preserve atrial function. Sinus rhythm helps to fill the left ventricle in late diastole and thus improve cardiac output. Preoperatively, the patient had been cardioverted and placed on an amiodarone infusion in an attempt to maintain sinus rhythm. Preoperatively, this patient presented for redo-OLT with a hyperdynamic left ventricle. However, not all patients with a hyperdynamic left ventricle develop SAM. The reported incidence of SAM after mitral valve repair is 8.4%.5 These patients, as with the present patient, do not have hypertrophy of the left ventricle musculature but may have abnormalities of their mitral valve anatomy such as elongation of either the anterior or posterior leaflet6 or a short coaptation-septal distance.7 Recently, with the introduction of 3-dimensional TEE, the contribution of anatomic abnormalities of the mitral valve in the production of SAM in the absence of septal hypertrophy can be better evaluated.8 In this patient, the preoperative transthoracic echocardiogram showed an anterior mitral leaflet measuring 3.2 cm, which is significantly longer than the average normal length of 2.5 cm. In a study of 17 patients with severe SAM, Mikami et al9 showed a surplus anterior mitral leaflet length of 0.9 ⫾ 0.2 cm. The present patient had a surplus length of 0.7 cm. This may suggest that in patients with end-stage liver disease, if the length of their mitral valve leaflets is more than normal, then they may be at risk of developing DLVOTO with SAM. The authors are now assessing the feasibility of requesting that the preoperative echocardiographic evaluation during the workup for patients listed for OLT include the length of mitral leaflets. In conclusion, the case of a patient who underwent redo-OLT with a known susceptibility for DLVOTO and SAM is presented. A prolonged anterior mitral valve leaflet may have contributed to this patient’s susceptibility. The management goals for this patient are presented. Because all patients undergo preoperative echocardiographic evaluation during their workup for OLT, the authors currently are assessing whether this measurement should be reported if possible, so that patients who may be susceptible for DLVOTO can be identified.
REFERENCES 1. Iwakiri Y, Groszmann RJ: The hyperdynamic circulation of chronic liver disease: From the patient to the molecule. Hepatology 43:121-131, 2006 (suppl) 2. Moller S, Henriksen JH: Cardiopulmonary complication in chronic liver disease. World J Gastroenterol 12:526-538, 2006 3. Aniskevich S, Shine TS, Feinglass NG, Stapelfeldt WH: Dynamic left ventricular outflow tract obstruction during liver transplant: The role of transesophageal echocardiography. J Cadiothorac Vasc Anesth 21:577-580, 2007 4. Cywinski JB, Argalious M, Marks TN, et al: Dynamic left ventricular outflow tract obstruction in an orthotopic liver transplant recipient. Liver Transpl 11:692-695, 2005 5. Brown ML, Abel MD, Click RL, et al: Systolic anterior motion after mitral valve repair. Is surgical intervention necessary? J Thorac Cardiovasc Surg 133:136-143, 2007
6. Cape EG, Simons D, Jimoh A, et al: Chordal geometry determines the shape and extent of systolic anterior motion: In vitro studies. J Am Coll Cardiol 13:1438-1448, 1989 7. Manecke GR, Nguyen LC, Tibble AD, et al: Systolic anterior motion after mitral valve repair and a systolic anterior motion tolerance test. J Cardiothorac Vasc Anesth 24:883-884, 2010 8. Jungwirth B, Adams DB, Mathew JP, et al: Mitral valve prolapse and systolic anterior motion illustrated by real time threedimensional transesophageal echocardiography. Anesth Analg 107: 1822-1824, 2008 9. Mikami T, Hashimoto M, Kudo T, et al: Mitral valve and its ring in hypertrophic cardiomyopathy: A mechanism creating surplus mitral leaflet involved in systolic anterior motion. Jpn Circ J 52:597-603, 1988
Anesthetic Management of a Patient With Dynamic Left Ventricular Outflow Tract Obstruction With Systolic Anterior Movement of the Mitral Valve Undergoing Redo–Orthotopic Liver Transplantation Debashis Roy, MD, and Fiona E. Ralley, MBChB, FRCA
E
ND-STAGE LIVER DISEASE is associated with significant hemodynamic changes.1,2 By the time patients present for liver transplantation, they often have a hyperdynamic circulation with a profound increase in their cardiac output (CO) and reduced systemic vascular resistance (SVR). This combination of hemodynamic derangements makes these patients especially prone to dynamic left ventricular outflow tract obstruction (DLVOTO). Aniskevich et al3 recently published a case report in which DVLOTO with systolic anterior motion (SAM) of the mitral valve was detected for the first time during the reperfusion phase of orthotopic liver transplantation (OLT) in a patient with an unremarkable preoperative cardiac evaluation and uneventful preanhepatic and anhepatic stages.3 A case of preoperative DLVOTO and SAM of the mitral valve with atrial fibrillation and significant hemodynamic instability presenting in a patient scheduled for redo-OLT is presented. The case was managed successfully with preoperative cardioversion to sinus rhythm and intraoperative hemodynamic management guided by transesophageal echocardiography (TEE). CASE REPORT The patient’s wife gave written consent to report this case. A 59-year-old man (108 kg, 177.5 cm) presented at the authors’ institution for redo-OLT. Fifteen years previously, he had undergone OLT for the treatment of cirrhosis secondary to hepatitis C virus and alcoholism. Over the previous 18 months, he had developed chronic rejection and was listed for redo-OLT. He had been scheduled to undergo redo-OLT, but at the last minute the organ was required by a more urgent recipient (in another province). However, because of his declining health, it was decided to keep the patient in the hospital for preoperative optimization. His past medical history was significant only for gout. Over the next few days, he developed
From the Department of Anesthesia and Perioperative Medicine, London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada. Address reprint requests to Fiona E. Ralley, MBChB, FRCA, Department of Anesthesia and Perioperative Medicine, LHSC University Hospital, Room C3-110, 339 Windermere Road, London, ON, Canada N6A 5A5. E-mail: [email protected] © 2012 Elsevier Inc. All rights reserved. 1053-0770/2602-0017$36.00/0 doi:10.1053/j.jvca.2011.02.014 Key words: liver transplantation, dynamic left ventricular outflow tract obstruction, systolic anterior motion of the mitral valve, transesophageal echocardiography 274
massive ascites, causing significant shortness of breath at rest. During the subsequent paracentesis, the patient became profoundly hypotensive. This was managed initially unsuccessfully with fluid resuscitation with albumin and a dopamine infusion for 2 to 3 days. Therefore, to rule out any cardiac abnormalities, transthoracic echocardiography was performed, which showed a hyperdynamic left ventricle with an ejection fraction of 80% and complete cavity obliteration during systole, left ventricular outflow tract obstruction with mean pressure gradient of 30 to 40 mmHg associated with severe SAM of the mitral valve, and moderate mitral regurgitation (Fig 1). The right side of the heart was normal. After extensive discussion among the anesthesiologists, the cardiologists, the transplant surgeons, and the patient’s family, it was decided that although it was high risk, redo-OLT was the only long-term option for this patient because the cardiac changes were dynamic with no intracardiac structural abnormalities. During the following 2 weeks while waiting for another suitable organ, the patient became more unstable. He developed hepatorenal syndrome with complete anuria and an increase in urea to 28.4 mmol/mL (80.39 mg/dL) and in creatinine to 403 mmol/mL (5.28 mg/dL). Because hemodialysis caused profound hypotension, he was started on continuous renal replacement therapy (PRISMA; Gambro Inc, Toronto, ON, Canada) 4 days before his subsequent transplant. At the same time, he developed hepatic encephalopathy secondary to a gastrointestinal bleed requiring transfer to the intensive care unit (ICU). His DVOTO was managed by an infusion of vasopressin (2.4 U/h) and by increasing his preload. Two days before his transplant, he developed atrial fibrillation, which was managed initially medically by maintaining his heart rate ⬍100 beats/min. Cardioversion was not considered at this time because it was felt unlikely to be successful or that the patient would not remain in sinus rhythm for any length of time. Furthermore, this would require that the patient be intubated before cardioversion because of his reduced conscious state and extubation would probably fail at that time. Immediately before transfer to the operating room for redo-OLT, he was intubated to protect his airway, cardioverted into sinus rhythm using 75 J, and started on amiodarone (a 150-mg bolus followed by an infusion of 1 mg/min) to try to maintain sinus rhythm. The preoperative laboratory testing showed a hemoglobin level of 83 mmol/mL, an international normalized ratio of 2.9, partial thromboplastin time of 67, and a platelet count of 26,000⫻109/L. After the induction of anesthesia with sufentanil, midazolam, and rocuronium, a left radial arterial catheter and the left internal jugular vein with a pulmonary catheter (right internal jugular vein was cannulated previously for dialysis) were inserted. Before surgical incision, the standard dose of 4.8 mg of recombinant activated factor VII (NovoSeven; Novo Nordisk Canada Inc, Mississauga, ON, Canada) was administered to try to reduce the bleeding during the prehepatic stage. The repeat international normalized ratio and partial thromboplastin time were 1.2 and 53, respectively.
Journal of Cardiothoracic and Vascular Anesthesia, Vol 26, No 2 (April), 2012: pp 274-276
DLVOTO IN REDO-OLT
275
Fig 1. Transthoracic echocardiography (parasternal long-axis view) showing the left ventricle during systole (complete obliteration of cavity) and SAM of the anterior mitral leaflet. LV, left ventricle; LA, left atrium; AO, aorta; MV, mitral valve; AV, aortic valve; AML, anterior mitral leaflet.
A transesophageal echocardiographic probe was inserted to monitor the cardiac function and to guide fluid administration. Table 1 describes the intraoperative problems, how they were managed, and the hemodynamic parameters. During the postreperfusion phase, the norepinephrine infusion was tapered slowly and discontinued, the vasopressin dose was reduced back to 2.4 U/h, and the phenylephrine dose was reduced to 40 g/min. The total operating time was 13 hours 40 minutes, with an estimated blood loss of ⬎20 L for which he received 42 U of packed red cells, 20 U of fresh frozen plasma, 10 U of platelets, 8 L of crystalloid, 1.5 L of colloid (Voluven; Fresenius Kabi Canada, Mississauga, ON, Canada), and 1 L of 5% albumin. After completion of surgery, the abdomen was packed open, and the patient was transferred to the ICU on vasopressin, 2.4 U/h, and phenylephrine, 40,g/min. Hemodynamic parameters at this time showed a heart rate of 88 beat/min, blood pressure of 102/56 mmHg, pulmonary arterial pressure of 39/21 mmHg, and a cardiac index of 7.4 L/m2/min. On the 3rd postoperative day (POD), with a well-functioning graft, the patient was returned to the operating room for removal of his
Fig 2. Transthoracic echocardiography (parasternal long-axis view) showing the left ventricle during systole and no SAM. LV, left ventricle; LA, left atrium; AO, aorta; MV, mitral valve; AV, aortic valve.
abdominal packs and formal wound closure. By POD 5, all vasopressor support had been discontinued, and on POD 9 repeat echocardiography showed no SAM, with normal left ventricular function and size, an ejection fraction of 67%, mild left atrial dilatation (4.9 cm), and a mildly dilated right ventricle (Fig 2). The patient was extubated on POD 14, and on POD 17 he was discharged from the ICU to the transplant unit. Renal function started to improve postoperatively, and by POD 45 dialysis was stopped. He was discharged home on POD 56. Unfortunately, after initially continuing to improve, his health gradually declined, and he died 16 months after his transplant. DISCUSSION
End-stage liver disease is associated with a hyperdynamic circulation leading to a profound increase in CO and a decrease in SVR.1,2 If there is a decrease in preload (eg, during bleeding, paracentesis, or cross-clamping of the inferior vena cava) or tachycardia (eg, during stress or reperfusion), then DLVOTO with SAM may be precipitated. In addition, during the reper-
Table 1. Intraoperative Problems, Management, and Outcomes Preanhepatic
Anhepatic (IVC XC ⫽ 67 min)
Reperfusion
Problems
DLVOTO with SAM secondary to massive blood loss from previous adhesions, portal hypertension, and coagulopathy
DLVOTO with SAM secondary to a decrease in venous return leading to a fall in preload
Management (titrated to maintain MBP ⬎70 mmHg and HR ⬍90 beats/min)
Phenylephrine (20-50 g/min) Amiodarone (1 mg/min) Esmolol (20-mg bolus) Massive blood transfusion Vasopressin infusion (4-8 U/h)
In addition to 1-5 of prehepatic norepinephrine (5-8 g/h)
DLVOTO with SAM secondary to release of toxin, interleukins, and complement factors from the donor’s liver and patient’s lower body Phenylephrine (up to max of 80 g/min) Amiodarone (1 mg/min) Vasopressin (up to max of 10 U/h) Norepinephrine (8 g/h)
Hemodynamics Heart rate (beats/min) IBP (mmHg) PAP (mmHg) CI (L/min/m2)
70-90 S 85-105 D 40-54 42/21-54/27 4.6-5.2
80-95 S 85-95 D 36-48 37/14-37/21 1.7-2.0
80-95 S 80-95 D 40-54 58/29 7.9
Abbreviations: IVC XC, inferior vena cava cross-clamp; HR, heart rate; IBP, invasive blood pressure; S, systolic; D, diastolic; MBP, mean blood pressure; PAP, pulmonary arterial pressure; CI, cardiac index.
276
ROY AND RALLEY
fusion stage of OLT, SVR may further be reduced, possibly also precipitating DLVOTO and SAM.3 The authors could find only 1 previous case report of DLVOTO without hypertrophy of the cardiac musculature.3 Aniskevich et al3 described a case in which they diagnosed DLVOTO by TEE during the reperfusion phase to assist in the diagnosis and management of refractory hypotension. Preoperative stress echocardiography and intraoperative preanhepatic and anhepatic phases had been unremarkable in this patient, and the authors postulated that the “loss of preload, coupled with the sudden drop in SVR, may have been enough to allow for a “perfect storm” in which a patient with a predisposition for DLVOTO may actually develop the obstruction.”3 Cywinski et al4 described a case in which DLVOTO was observed during preoperative stress echocardiography with normal hemodynamics. However, this patient had left ventricular hypertrophy with septal hypertrophy and only developed mild hemodynamic instability during the reperfusion stage, which was managed with low-dose vasopressor support. This case report differs from these previous case reports because the present patient developed preoperative DLVOTO with SAM without any obvious precipitating stress. Preoperatively, he was hemodynamically unstable requiring vasopressor support. At present, there are no clear guidelines for the management of these patients requiring OLT. Therefore, before the start of the case, the authors established 4 goals. The 1st goal was to maintain preload, especially during the dissection phase, when there was likely to be profound blood loss secondary to the adhesion from his previous OLT, his significant portal hypertension, and the concurrent coagulopathy. The rapid replacement of blood products was achieved with the use of a level 1 rapid infusion system (SIMS Level 1 Inc, Rockland, MA) and was guided by TEE and/or pulmonary arterial pressure. The 2nd goal was to maintain afterload by preventing any reduction in the SVR using phenylephrine, vasopressin, and norepinephrine. The 3rd goal was to avoid tachycardia, for which esmolol boluses were used to maintain a heart rate ⬍90 beats/min. The
4th goal was to preserve atrial function. Sinus rhythm helps to fill the left ventricle in late diastole and thus improve cardiac output. Preoperatively, the patient had been cardioverted and placed on an amiodarone infusion in an attempt to maintain sinus rhythm. Preoperatively, this patient presented for redo-OLT with a hyperdynamic left ventricle. However, not all patients with a hyperdynamic left ventricle develop SAM. The reported incidence of SAM after mitral valve repair is 8.4%.5 These patients, as with the present patient, do not have hypertrophy of the left ventricle musculature but may have abnormalities of their mitral valve anatomy such as elongation of either the anterior or posterior leaflet6 or a short coaptation-septal distance.7 Recently, with the introduction of 3-dimensional TEE, the contribution of anatomic abnormalities of the mitral valve in the production of SAM in the absence of septal hypertrophy can be better evaluated.8 In this patient, the preoperative transthoracic echocardiogram showed an anterior mitral leaflet measuring 3.2 cm, which is significantly longer than the average normal length of 2.5 cm. In a study of 17 patients with severe SAM, Mikami et al9 showed a surplus anterior mitral leaflet length of 0.9 ⫾ 0.2 cm. The present patient had a surplus length of 0.7 cm. This may suggest that in patients with end-stage liver disease, if the length of their mitral valve leaflets is more than normal, then they may be at risk of developing DLVOTO with SAM. The authors are now assessing the feasibility of requesting that the preoperative echocardiographic evaluation during the workup for patients listed for OLT include the length of mitral leaflets. In conclusion, the case of a patient who underwent redo-OLT with a known susceptibility for DLVOTO and SAM is presented. A prolonged anterior mitral valve leaflet may have contributed to this patient’s susceptibility. The management goals for this patient are presented. Because all patients undergo preoperative echocardiographic evaluation during their workup for OLT, the authors currently are assessing whether this measurement should be reported if possible, so that patients who may be susceptible for DLVOTO can be identified.
REFERENCES 1. Iwakiri Y, Groszmann RJ: The hyperdynamic circulation of chronic liver disease: From the patient to the molecule. Hepatology 43:121-131, 2006 (suppl) 2. Moller S, Henriksen JH: Cardiopulmonary complication in chronic liver disease. World J Gastroenterol 12:526-538, 2006 3. Aniskevich S, Shine TS, Feinglass NG, Stapelfeldt WH: Dynamic left ventricular outflow tract obstruction during liver transplant: The role of transesophageal echocardiography. J Cadiothorac Vasc Anesth 21:577-580, 2007 4. Cywinski JB, Argalious M, Marks TN, et al: Dynamic left ventricular outflow tract obstruction in an orthotopic liver transplant recipient. Liver Transpl 11:692-695, 2005 5. Brown ML, Abel MD, Click RL, et al: Systolic anterior motion after mitral valve repair. Is surgical intervention necessary? J Thorac Cardiovasc Surg 133:136-143, 2007
6. Cape EG, Simons D, Jimoh A, et al: Chordal geometry determines the shape and extent of systolic anterior motion: In vitro studies. J Am Coll Cardiol 13:1438-1448, 1989 7. Manecke GR, Nguyen LC, Tibble AD, et al: Systolic anterior motion after mitral valve repair and a systolic anterior motion tolerance test. J Cardiothorac Vasc Anesth 24:883-884, 2010 8. Jungwirth B, Adams DB, Mathew JP, et al: Mitral valve prolapse and systolic anterior motion illustrated by real time threedimensional transesophageal echocardiography. Anesth Analg 107: 1822-1824, 2008 9. Mikami T, Hashimoto M, Kudo T, et al: Mitral valve and its ring in hypertrophic cardiomyopathy: A mechanism creating surplus mitral leaflet involved in systolic anterior motion. Jpn Circ J 52:597-603, 1988