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Vasoplegic syndrome during Whipple procedure
Journal of Clinical Anesthesia 36 (2017) 151–152
Contents lists available at ScienceDirect
Journal of Clinical Anesthesia
Case Report
Vasoplegic syndrome during Whipple procedure☆ Tejesh C. Anandaswamy, MD (Associate Professor) a,⁎, Geetha C. Rajappa, DNB (Associate Professor) a, Harish Krishnamachar, MCh(Professor) b a b
Department of Anaesthesiology, MS Ramaiah Medical College and Hospitals, Bangalore, India Department of Surgical Oncology, MS Ramaiah Medical College and Hospitals, Bangalore, India
a r t i c l e
i n f o
Article history: Received 31 August 2015 Received in revised form 14 October 2016 Accepted 30 October 2016 Available online xxxx Keywords: Noncardiac surgery Vasoplegic syndrome Topic: Vasopressin
a b s t r a c t Vasoplegic syndrome is an unusual cause of refractory hypotension under general anesthesia. It is commonly described in the setting of cardiac surgery, but rarely seen in noncardiac setting. We describe successful management of vasoplegic syndrome during Whipple procedure with vasopressin infusion. A high index of suspicion and prompt treatment with vasopressin can be lifesaving in patients with risk factors for vasoplegic syndrome who present with severe refractory hypotension and who respond poorly to fluid administration and routine vasopressor infusion. © 2016 Elsevier Inc. All rights reserved.
1. Introduction Vasoplegic syndrome is a severe vasodilatory shock characterized by hypotension, tachycardia, and normal or elevated cardiac output, decrease in systemic vascular resistance, poor or no response to fluid resuscitation, and vasopressor administration [1]. Although it is commonly seen during cardiac surgery, it is also been reported during noncardiac surgery [2,3]. The incidence of vasoplegic syndrome is 8%10% in cardiac surgery [4], and its risk factors include intravenous heparin, β-blockers, calcium channel blockers, renin-angiotensin system antagonists, protamine use, myocardial dysfunction, diabetes mellitus, presence of precardiopulmonary bypass hemodynamic instability, increased duration of cardiopulmonary bypass, and ventricular device insertion [5]. We present a case of successful management of vasoplegic syndrome that developed perioperatively after Whipple procedure. 2. Case report A 76-year-old, 52-kg man was schedule for Whipple procedure for carcinoma head of pancreas. He was a known hypertensive of enalapril and poorly controlled diabetic on insulin. His preoperative investigations were unremarkable except of elevated hemoglobin A1C. The proposed procedure was planned under general anesthesia with thoracic ☆ Disclosures: None to declare. ⁎ Corresponding author at: Department of Anaesthesiology, MS Ramaiah Medical College and Hospitals, Bangalore 560054, India. Tel.:+91 9886481848. E-mail address: [email protected] (T.C. Anandaswamy).
http://dx.doi.org/10.1016/j.jclinane.2016.10.042 0952-8180/© 2016 Elsevier Inc. All rights reserved.
epidural, for which the patient consented. After instituting appropriate monitoring, thoracic epidural catheter was placed in T7-T8 interspace before induction of general anesthesia. General anesthesia was induced with fentanyl 2 μg/kg and propofol 2 mg/kg, and intubation was facilitated with vecuronium 0.1 mg/kg. After induction of general anesthesia, left radial artery and right subclavian vein were cannulated for invasive blood pressure and central venous pressure monitoring. Patient had an uneventful intraoperative course till about 3 hours into the intraoperative period when a gradual fall in blood pressure to 60/40 mm Hg and tachycardia (heart rate,110-120 bpm) was noted despite central venous pressure being maintained between 10 and 14 cm H2O and only about 300 mL of operative blood loss. The reduction in systolic pressure did not respond to crystalloid fluid boluses. Hence, a decision was made to start dopamine and noradrenaline. Blood pressure did not improve more than 65-70/40 mm Hg (mean arterial pressure, 45-50 mm Hg) despite increasing the dose of dopamine and noradrenaline and heart rate ranged from 130-140 bpm. Also, ST depression was noted in electrocardiogram on the multiparameter monitor. The surgery was completed within the next 60 minutes. In view of persistent hypotension not responding to dopamine (20 μg/kg/min) and noradrenaline (0.5-1 μg/kg/min), vasopressin at 1 U/h was started. After vasopressin infusion, his blood pressure improved over the next 30-45 minutes and it ranged between 100/50 and 110/50 mm Hg (mean arterial pressure, 65-70 mm Hg) and the heart rate reduced to 90-100 bpm. As the patient was hemodynamically unstable, epidural was not activated and was shifted to intensive care unit for postoperative ventilatory support and further management. Suspecting myocardial ischemia, an echocardiography which was done in the immediate postoperative period was
152
T.C. Anandaswamy et al. / Journal of Clinical Anesthesia 36 (2017) 151–152
unremarkable with an ejection fraction of 58%, good ventricular filling, and no regional wall motion abnormalities. Also, troponin T levels were within normal limits. Over the next 36 hours, patient was gradually weaned of both the ventilator support (on fentanyl infusion at 25-30 μg/h continuous infusion) and vasopressor support. His further hospital course was uneventful and was discharged home on the 10th postoperative day. 3. Discussion Vasoplegic syndrome is a severe refractory hypotension seen more commonly during cardiac surgery, but can occur during any anesthetic. Vasoplegic syndrome is usually defined as a mean arterial pressure less than 50 mm Hg with a cardiac index greater than 2.5 L/min/m2 and a low systemic vascular resistance despite adrenergic vasopressor administration (noradrenaline infusion, ≥0.5 μg/kg/min) [1,2,6]. The incidence of vasoplegic syndrome is 8%-10% in cardiac surgery [5], and its risk factors include intravenous heparin, β-blockers, calcium channel blockers, reninangiotensin system antagonists, protamine use, myocardial dysfunction, diabetes mellitus, presence of precardiopulmonary bypass hemodynamic instability, increased duration of cardiopulmonary bypass, and ventricular device insertion [5]. Clinically, patients have persistent hypotension, tachycardia, normal oxygen saturation, and poor or no response to intravascular volume expansion and vasoconstrictive agents [1,6,7]. In the present case, patient's blood pressure remained at 60/40 mm Hg despite central venous pressure being 10-14 cm H2O and crystalloid fluid administration. Even after initiation of infusion of dopamine and noradrenaline, there was no improvement in blood pressure. Patient's blood pressure improved only on starting vasopressin administration. Vasoplegic syndrome is rarely reported in the setting of noncardiac surgery. Cao et al [3] have reported successful treatment of vasoplegic syndrome during neohepatic phase of liver transplantation. We did not know our patient's cardiac output or systemic vascular resistance, whereas, it is routinely monitored in cardiac surgery and liver transplantation. Our patient was on renin-angiotensin antagonist and was a diabetic, which are among the known risk factors for vasoplegic syndrome. Physiologically, blood pressure is maintained by the sympathetic, reninangiotensin, and vasopressinergic systems. Under general anesthesia, the influence of sympathetic system on cardiovascular tone is reduced, and hence, there is increased reliance on renin-angiotensin and vasopressinergic systems to maintain blood pressure [8]. Reninangiotensin antagonists block the response of renin-angiotensin system response to hypotension. Hence, patients on these agents are at risk of refractory hypotension under general anesthesia [2]. Other proposed mechanisms for vasoplegic syndrome are cytokine and nitric oxide– mediated smooth muscle relaxation, catecholamine receptor down regulation, cell hyperpolarization, and endothelial injury [9]. The present
case, in which refractory shock was responsive only to vasopressin, highlights the need to entertain vasoplegic syndrome as one of the causes of refractory hypotension under general anesthesia in patients on rennin angiotensin antagonists. Vasopressin is an endogenous hormone formed in the supraoptic nuclei of the hypothalamus and secreted by the posterior pituitary. Vasopressin is found to be deficient in patients with vasoplegic syndrome and is the rationale for its use [10]. It is not clear if plasma levels of vasopressin can be used as a biochemical marker for vasoplegic syndrome. The treatment of vasoplegic syndrome is challenging and when treatments such as decreasing the anesthetic agent, volume expansion, phenylephrine, norepinephrine, and epinephrine are not effective, exogenous vasopressin may improve hypotension.2 Methylene blue is also an alternative for treatment of vasoplegic syndrome [2,6]. It is believed to interfere with nitric oxide-cGMP pathway, thereby inhibiting the vasorelaxant effect of nitric oxide on vascular smooth muscle [6,9]. Vasoplegic syndrome is an unusual complication during noncardiac surgery. A high index of suspicion and prompt treatment with vasopressin can be lifesaving in patients with risk factors for vasoplegic syndrome who present with severe refractory hypotension and who respond poorly to fluid administration and routine vasopressor infusion. Acknowledgments None. References [1] Gomes WJ, Carvahlo AC, Palms JH, Teles CA, Branco JN, Silas MG, et al. Vasoplegic syndrome after open heart surgery. J Cardiovasc Surg (Torino) 1998;39:619–23. [2] Shear T, Greenberg S. Vasoplegic syndrome and renin-angiotensin system antagonists. APSF Newsl 2012;27:18–9. [3] Cao Z, Gao Y, Tao G. Vasoplegic syndrome during liver transplantation. Anesth Analg 2009;108:1941–3. [4] Mekontso-Dessap A, Houel R, Soustelle C, Kirsch M, Thebert D, Loisance DY. Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function. Ann Thorac Surg 2001;71:1428–32. [5] Fischer GW, Levin MA. Vasoplegia during cardiac surgery: current concepts and management. Semin Thorac Cardiovasc Surg 2010;22:140–4. [6] Shanmugan G. Vasoplegic syndrome—the role of methylene blue. Eur J Cardiothorac Surg 2005;28:705–10. [7] Gomes WJ, Erlichman MR, Batista-Filho ML, Knobel M, Almeida DR, Carvalho AC, et al. Vasoplegic syndrome after off-pump coronary artery bypass surgery. Eur J Cardiothorac Surg 2003;23:165–9. [8] Lange M, Aken HV, Westphal M, Morelli A. Role of vasopressinergic V1 receptor agonists in the treatment of perioperative catecholamine-refractory arterial hypotension. Best Pract Res Clin Anaesthesiol 2008;22:369–81. [9] Lavigne D. Vasopressin and methylene blue: alternate therapies in vasodilatory shock. Semin Cardiothorac Vasc Anesth 2010;14:186–9. [10] Raja SG, Dreyfus GD. Vasoplegic syndrome after off-pump coronary artery bypass surgery. An unusual complication. Tex Heart Inst J 2004;31:421–4.
Contents lists available at ScienceDirect
Journal of Clinical Anesthesia
Case Report
Vasoplegic syndrome during Whipple procedure☆ Tejesh C. Anandaswamy, MD (Associate Professor) a,⁎, Geetha C. Rajappa, DNB (Associate Professor) a, Harish Krishnamachar, MCh(Professor) b a b
Department of Anaesthesiology, MS Ramaiah Medical College and Hospitals, Bangalore, India Department of Surgical Oncology, MS Ramaiah Medical College and Hospitals, Bangalore, India
a r t i c l e
i n f o
Article history: Received 31 August 2015 Received in revised form 14 October 2016 Accepted 30 October 2016 Available online xxxx Keywords: Noncardiac surgery Vasoplegic syndrome Topic: Vasopressin
a b s t r a c t Vasoplegic syndrome is an unusual cause of refractory hypotension under general anesthesia. It is commonly described in the setting of cardiac surgery, but rarely seen in noncardiac setting. We describe successful management of vasoplegic syndrome during Whipple procedure with vasopressin infusion. A high index of suspicion and prompt treatment with vasopressin can be lifesaving in patients with risk factors for vasoplegic syndrome who present with severe refractory hypotension and who respond poorly to fluid administration and routine vasopressor infusion. © 2016 Elsevier Inc. All rights reserved.
1. Introduction Vasoplegic syndrome is a severe vasodilatory shock characterized by hypotension, tachycardia, and normal or elevated cardiac output, decrease in systemic vascular resistance, poor or no response to fluid resuscitation, and vasopressor administration [1]. Although it is commonly seen during cardiac surgery, it is also been reported during noncardiac surgery [2,3]. The incidence of vasoplegic syndrome is 8%10% in cardiac surgery [4], and its risk factors include intravenous heparin, β-blockers, calcium channel blockers, renin-angiotensin system antagonists, protamine use, myocardial dysfunction, diabetes mellitus, presence of precardiopulmonary bypass hemodynamic instability, increased duration of cardiopulmonary bypass, and ventricular device insertion [5]. We present a case of successful management of vasoplegic syndrome that developed perioperatively after Whipple procedure. 2. Case report A 76-year-old, 52-kg man was schedule for Whipple procedure for carcinoma head of pancreas. He was a known hypertensive of enalapril and poorly controlled diabetic on insulin. His preoperative investigations were unremarkable except of elevated hemoglobin A1C. The proposed procedure was planned under general anesthesia with thoracic ☆ Disclosures: None to declare. ⁎ Corresponding author at: Department of Anaesthesiology, MS Ramaiah Medical College and Hospitals, Bangalore 560054, India. Tel.:+91 9886481848. E-mail address: [email protected] (T.C. Anandaswamy).
http://dx.doi.org/10.1016/j.jclinane.2016.10.042 0952-8180/© 2016 Elsevier Inc. All rights reserved.
epidural, for which the patient consented. After instituting appropriate monitoring, thoracic epidural catheter was placed in T7-T8 interspace before induction of general anesthesia. General anesthesia was induced with fentanyl 2 μg/kg and propofol 2 mg/kg, and intubation was facilitated with vecuronium 0.1 mg/kg. After induction of general anesthesia, left radial artery and right subclavian vein were cannulated for invasive blood pressure and central venous pressure monitoring. Patient had an uneventful intraoperative course till about 3 hours into the intraoperative period when a gradual fall in blood pressure to 60/40 mm Hg and tachycardia (heart rate,110-120 bpm) was noted despite central venous pressure being maintained between 10 and 14 cm H2O and only about 300 mL of operative blood loss. The reduction in systolic pressure did not respond to crystalloid fluid boluses. Hence, a decision was made to start dopamine and noradrenaline. Blood pressure did not improve more than 65-70/40 mm Hg (mean arterial pressure, 45-50 mm Hg) despite increasing the dose of dopamine and noradrenaline and heart rate ranged from 130-140 bpm. Also, ST depression was noted in electrocardiogram on the multiparameter monitor. The surgery was completed within the next 60 minutes. In view of persistent hypotension not responding to dopamine (20 μg/kg/min) and noradrenaline (0.5-1 μg/kg/min), vasopressin at 1 U/h was started. After vasopressin infusion, his blood pressure improved over the next 30-45 minutes and it ranged between 100/50 and 110/50 mm Hg (mean arterial pressure, 65-70 mm Hg) and the heart rate reduced to 90-100 bpm. As the patient was hemodynamically unstable, epidural was not activated and was shifted to intensive care unit for postoperative ventilatory support and further management. Suspecting myocardial ischemia, an echocardiography which was done in the immediate postoperative period was
152
T.C. Anandaswamy et al. / Journal of Clinical Anesthesia 36 (2017) 151–152
unremarkable with an ejection fraction of 58%, good ventricular filling, and no regional wall motion abnormalities. Also, troponin T levels were within normal limits. Over the next 36 hours, patient was gradually weaned of both the ventilator support (on fentanyl infusion at 25-30 μg/h continuous infusion) and vasopressor support. His further hospital course was uneventful and was discharged home on the 10th postoperative day. 3. Discussion Vasoplegic syndrome is a severe refractory hypotension seen more commonly during cardiac surgery, but can occur during any anesthetic. Vasoplegic syndrome is usually defined as a mean arterial pressure less than 50 mm Hg with a cardiac index greater than 2.5 L/min/m2 and a low systemic vascular resistance despite adrenergic vasopressor administration (noradrenaline infusion, ≥0.5 μg/kg/min) [1,2,6]. The incidence of vasoplegic syndrome is 8%-10% in cardiac surgery [5], and its risk factors include intravenous heparin, β-blockers, calcium channel blockers, reninangiotensin system antagonists, protamine use, myocardial dysfunction, diabetes mellitus, presence of precardiopulmonary bypass hemodynamic instability, increased duration of cardiopulmonary bypass, and ventricular device insertion [5]. Clinically, patients have persistent hypotension, tachycardia, normal oxygen saturation, and poor or no response to intravascular volume expansion and vasoconstrictive agents [1,6,7]. In the present case, patient's blood pressure remained at 60/40 mm Hg despite central venous pressure being 10-14 cm H2O and crystalloid fluid administration. Even after initiation of infusion of dopamine and noradrenaline, there was no improvement in blood pressure. Patient's blood pressure improved only on starting vasopressin administration. Vasoplegic syndrome is rarely reported in the setting of noncardiac surgery. Cao et al [3] have reported successful treatment of vasoplegic syndrome during neohepatic phase of liver transplantation. We did not know our patient's cardiac output or systemic vascular resistance, whereas, it is routinely monitored in cardiac surgery and liver transplantation. Our patient was on renin-angiotensin antagonist and was a diabetic, which are among the known risk factors for vasoplegic syndrome. Physiologically, blood pressure is maintained by the sympathetic, reninangiotensin, and vasopressinergic systems. Under general anesthesia, the influence of sympathetic system on cardiovascular tone is reduced, and hence, there is increased reliance on renin-angiotensin and vasopressinergic systems to maintain blood pressure [8]. Reninangiotensin antagonists block the response of renin-angiotensin system response to hypotension. Hence, patients on these agents are at risk of refractory hypotension under general anesthesia [2]. Other proposed mechanisms for vasoplegic syndrome are cytokine and nitric oxide– mediated smooth muscle relaxation, catecholamine receptor down regulation, cell hyperpolarization, and endothelial injury [9]. The present
case, in which refractory shock was responsive only to vasopressin, highlights the need to entertain vasoplegic syndrome as one of the causes of refractory hypotension under general anesthesia in patients on rennin angiotensin antagonists. Vasopressin is an endogenous hormone formed in the supraoptic nuclei of the hypothalamus and secreted by the posterior pituitary. Vasopressin is found to be deficient in patients with vasoplegic syndrome and is the rationale for its use [10]. It is not clear if plasma levels of vasopressin can be used as a biochemical marker for vasoplegic syndrome. The treatment of vasoplegic syndrome is challenging and when treatments such as decreasing the anesthetic agent, volume expansion, phenylephrine, norepinephrine, and epinephrine are not effective, exogenous vasopressin may improve hypotension.2 Methylene blue is also an alternative for treatment of vasoplegic syndrome [2,6]. It is believed to interfere with nitric oxide-cGMP pathway, thereby inhibiting the vasorelaxant effect of nitric oxide on vascular smooth muscle [6,9]. Vasoplegic syndrome is an unusual complication during noncardiac surgery. A high index of suspicion and prompt treatment with vasopressin can be lifesaving in patients with risk factors for vasoplegic syndrome who present with severe refractory hypotension and who respond poorly to fluid administration and routine vasopressor infusion. Acknowledgments None. References [1] Gomes WJ, Carvahlo AC, Palms JH, Teles CA, Branco JN, Silas MG, et al. Vasoplegic syndrome after open heart surgery. J Cardiovasc Surg (Torino) 1998;39:619–23. [2] Shear T, Greenberg S. Vasoplegic syndrome and renin-angiotensin system antagonists. APSF Newsl 2012;27:18–9. [3] Cao Z, Gao Y, Tao G. Vasoplegic syndrome during liver transplantation. Anesth Analg 2009;108:1941–3. [4] Mekontso-Dessap A, Houel R, Soustelle C, Kirsch M, Thebert D, Loisance DY. Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function. Ann Thorac Surg 2001;71:1428–32. [5] Fischer GW, Levin MA. Vasoplegia during cardiac surgery: current concepts and management. Semin Thorac Cardiovasc Surg 2010;22:140–4. [6] Shanmugan G. Vasoplegic syndrome—the role of methylene blue. Eur J Cardiothorac Surg 2005;28:705–10. [7] Gomes WJ, Erlichman MR, Batista-Filho ML, Knobel M, Almeida DR, Carvalho AC, et al. Vasoplegic syndrome after off-pump coronary artery bypass surgery. Eur J Cardiothorac Surg 2003;23:165–9. [8] Lange M, Aken HV, Westphal M, Morelli A. Role of vasopressinergic V1 receptor agonists in the treatment of perioperative catecholamine-refractory arterial hypotension. Best Pract Res Clin Anaesthesiol 2008;22:369–81. [9] Lavigne D. Vasopressin and methylene blue: alternate therapies in vasodilatory shock. Semin Cardiothorac Vasc Anesth 2010;14:186–9. [10] Raja SG, Dreyfus GD. Vasoplegic syndrome after off-pump coronary artery bypass surgery. An unusual complication. Tex Heart Inst J 2004;31:421–4.