Begin typing your search above and press return to search.
Volume: 14 Issue: 2 April 2016

FULL TEXT

CASE REPORT
Anesthesia Management in Aortic Dissection in Patients Undergoing Kidney Transplant

Kidney transplant is a last resort to increase the life expectancy and quality of life in patients with renal failure. Aortic dissection is a disease that requires emergency intervention; it is characterized by sudden life-threatening back or abdominal pain. In the case described, constant chest pain that increased with respiration was present on exam-ination of a 28-year-old man (85 kg, 173 cm) who presented at our emergency department complaining of severe back pain. He had undergone a kidney transplant in 2004 from his mother (live donor). He was diagnosed with acute Type II aortic dissection and was scheduled for emergent surgery. Because there were no surgical or anesthetic complications, the patient with 79 and 89 minutes aortic cross-clamping and cardiopulmonary bypass durations was sent, intubated, to intensive care unit. When nephrotoxic agents are avoided and blood flow is stabilized, cardiovascular surgery with cardio-pulmonary bypass may be performed seamlessly in patients who have undergone a kidney transplant.


Key words : Anesthesia, Aortic surgery, Renal transplanted patients, Complications

Introduction

Kidney transplant is a last resort to increase the life expectancy and quality of life in patients with renal failure1; they can expect a prolonged and comfortable life.2 In patients who have undergone a kidney transplant, cardiovascular diseases are the main causes for morbidity and mortality.3 Although nephrotoxic agents should be avoided in all patients, those patients who already have had a renal transplant should be particularly careful.

Aortic dissection requires emergency intervention; it is characterized by sudden life-threatening back or abdominal pain. The disease is more frequently seen in women over the age of 50 years.4 In the current case, we sought to present a method of anesthesia and review the points that should be considered in a patient who has undergone successful surgery for a kidney transplant with a concomitant ascending aorta aneurism.

Case Report

On physical examination, a 28-year-old man (85 kg, 173 cm) presented at the emergency department with severe back pain and constant chest pain that increased with respiration. In 2004, he had undergone a kidney transplant from his mother (live donor). Hematology examination included hemoglobin 130 g/L, hematocrit 0.39, and proportion of 1.0 his biochemistry results were 118.95 μmol/L; blood urea nitrogen (BUN) was 10.71 mmol/L; and sodium and potassium values were normal. He had hypertension. On echocardiography, his ejection fraction was 60%, and he had normal left ventricle systolic functions, second-degree aorta failure, flap in ascending aorta, and pericardial effusion. A computed tomographic image of the thorax exhibited the diameter of the proximal ascending aorta was 65 mm and the intimal flap.

He was diagnosed as having acute type II aortic dissection, and he was scheduled for an emergency operation. Before admission to the operating suite and subsequent induction of anesthesia, the patient was monitored for electrocardiography vein cannulation and pulse oximetry. Because his pulse oximetry was eighty-nine, 5 L/min-1 oxygen was begun. Cannulation of the veins in both arms was accomplished with 16-gauge cannulas; local anesthesia was done with 1% lidocaine, and arterial cannulation from the left radial artery was done with a 20-gauge cannula. Input pressure was 145/85 mm Hg, and his pulse was 90 beats/minute. Anesthesia was induced with propofol 2 mg/kg, fentanyl 2 to 3 μ/kg, and 0.1 mg/kg vecuronium. Respiration was done with manual ventilation (O2 100%) to the neuromuscular junction. Mechanical ventilation was applied to provide end tidal CO2 volume of 35 to 40 mm Hg; FiO2, 40%; tidal volume, 6 to 8 mL/kg-1; and respiratory rate 10 to 12.

After anesthesia induction, the patient was given 1 g cephazolin sodium and 20 mg methylprednisolone intravenously. After anesthesia induction, central catheterization was performed through the right internal jugular vein. Anesthesia was maintained with fentanyl and sevoflurane. Fentanyl 3 μ/kg was applied before the incision, before the sternotomy, and at the beginning of cardiopulmonary bypass (CPB). One to 5 μ/kg of additional fentanyl was given to maintain a mean arterial pressure of > 100 mm Hg until cannulation, > 80 mm Hg during cannulation, and > 100 mm Hg after CPB. Sevoflurane con-centration was adjusted to 0.5% to 2% under the same criteria. Arterial cannulation was done from the right axillary artery. After a median sternotomy, venous cannulation was performed at the right atrial appendix. Descending aorta was seen to be aneurysmatic, and the dissection was limited to the ascending aorta. Aortic cross-clamping was done to an intact aorta, proximal to the innominate artery. Nitrous oxide was not used during induction and maintenance of anesthesia.

At first, a proximal anastomosis of the ascending aorta was performed with a graft. Then, when the aorta was evaluated for a distal aortic anastomosis, a distal aortic anastomosis was performed without circulatory arrest to restrict dissection of the ascending aorta and no upward movement of the flap. Because there were no surgical or anesthetic complications, the patient with 79 and 89 minutes aortic cross-clamping and CPB durations was sent, intubated, to intensive care unit. The patient was extubated 4 hours after surgery. At 1 day after surgery, his creatinine concentration was 199.78 μmol/L and his BUN was 16.78 mmol/L; 2 days after surgery, his creatinine concentration was 164.70 μmol/L and his BUN was 20.35 mmol/L; 3 days after surgery his creatinine concentration was 132.68 μmol/L and his BUN was 13.21 mmol/L; finally, the patient was discharged home 7 days after surgery.

Discussion

Kidney transplant is the most effective treatment for patients with terminal kidney disease. Factors including hypertension, abnormal lipid metabolism, diabetes mellitus, and immunosuppressive treatment accelerate cardiovascular disease in patients with renal transplant. In the literature, increases in cardiomyopathy, valvular lesions, calcified vein diseases, and peripheral vascular diseases with hypertension are reported in kidney, pancreas, or kidney and pancreas transplant recipients.5 Cardiovascular diseases are responsible for approximately 30% of deaths after renal transplants; 40% of these are within 3 months.6,7 Aortic dissection develops in only 2 patients/month after a successful renal transplant, and cardiovascular surgeries generally are done at a later time.8-10 Aortic dissection is a condition arising because of an accumulation of blood in the media after forming a tear in the aortic intima. Because a fatal rupture or cardiac tamponade may form at any time, treatment of acute proximal aortic dissection is an emergent condition.

Although preoperative weak renal function is known to be the most important risk factor for developing postoperative renal failure, the type of surgery also is important. Developing acute tubular necrosis after a vascular operation consisting of suprarenal aorta cross-clamping, thoracic, or thoraco-abdominal aortic surgery is similar, and death in patients requiring renal replacement therapy after whole aortic surgery is nearly 64% in the short term.11-13 Therefore, when patient undergoing anesthesia is at high risk, it is critical to avoid potentially nephrotoxic agents. In our patient, we used propofol, fentanyl, and vecuronium to induce anesthesia. Propofol and vecuronium are metabolized mainly in the liver, and their eliminations are independent from the renal function. However, metabolite and partial prototype of vecuronium is excreted by the kidneys. Our patient was extubated 4 hours after surgery. Additionally, because our patient had been using steroids for a long time after transplant, intraoperative methylprednisolone was administered.

All inhalation agents reduce renal blood flow and glomerular filtration rate in a dose-dependent manner. Therefore, it is crucial to provide renal perfusion. Compound A is formed because of a chemical reaction between sevoflurane and absorbent carbon dioxide. Although a hazardous effect of compound A has been shown in rabbits, this effect has not been shown in humans until now.14 On the contrary, in a previous study, sevoflurane has been shown to be at least as safe as isoflurane and desflurane.15,16 Therefore, we used sevoflurane to maintain anesthesia in our patient.

Reasons for developing renal dysfunction after CPB include surgical trauma, blood transfusion, elevation in proinflammatory cytokines with anesthesia, activation of the complement with heparin-protamine interaction, factors related to bypass, contact activation, ischemia, and endotoxin translocation.11 In our patient, while on CPB, his hemoglobin level was 8 g/dL and his hematocrit was 30%. Therefore, we did not perform any blood transfusions. Additionally, oliguria may be present when a decrease in the kidney perfusion pressure of if angiotensin-converting-enzyme inhibitors were used. Our patient had been using angiotensin-converting-enzyme inhibitors for 3 years. No significant decrease was present in mean arterial pressure both after induction and during maintenance.

Kim and associates17 reported in their retro-spective observational studies that a decrease in the preoperative left ventricle systolic function, prolonged operative time, intraoperative furosemide use, intraoperative oliguria after graft replacement in patients above 60 years, and decreases in the preoperative level of glomerular filtration rate were independent risk factors, respecting the incidence of postoperative acute kidney injury and increased short-term death. In our patient, the operative time was 4.5 hours, and aortic cross-clamping and CPB periods were 79 and 89 minutes. Forty mg furosemide and 150 mL 20% mannitol was placed in the prime solution of our patient, and urination was more than 0.5 mL/kg/hours. His BUN and creatinine levels during the postoperative period were normal. Additionally, unlike the study in which Musci and associates retrospectively examined heart valve operations in solid-organ recipients, no serious infection was formed in our patient, and he was discharged with good clinical results.10

Consequently, we believe that when potentially nephrotoxic agents are avoided and hemodynamics directed to target are provided, major cardiovascular surgery with CPB may be performed seamlessly in patients who have undergone a kidney transplant as renal functions are preserved.


References:

  1. Küçükarslan N, Süngün M, Us MH, et al. Off-pump coronary artery bypass operation in a renal transplant patient [in Turkish]. Anadolu Kardiyol Derg. 2006;6(2):193-194.
    PubMed
  2. Kara İ, Çelik G. Anesthesia management in patient with renal transplant [in Turkish]. Selçuk Tıp Derg. 2013;29(2):100-104.
  3. Tezcaner T, Yorgancioğlu C, Moldibi O, Çatav Z, Zorlutuna IY. Coronary bypass surgery in a renal transplant patient. Türk Nefroloji Diyaliz ve Transplantasyon Dergisi'Official Journal of the Turkish Nephrology, Association. 1996;3:127-129.
  4. Yağmur F, Din H, Özbek A, Kaya M. Sudden death due to rupture of dissection of the aorta: three cases. Düzce Tıp Dergisi. 2010;12(3):68-71.
  5. Wang LW, Fahim MA, Hayen A, et al. Cardiac testing for coronary artery disease in potential kidney transplant recipients: a systematic review of test accuracy studies. Am J Kidney Dis. 2011;57(3):476-487.
    CrossRef - PubMed
  6. Boschiero L, Fior F, Nacchia F. Bimodal distribution of major cardiovascular events in kidney allograft recipients. Transplant Proc. 2009;41(4):1183-1186.
    CrossRef - PubMed
  7. Aalten J, Hoogeveen EK, Roodnat JI, et al. Associations between pre-kidney-transplant risk factors and post-transplant cardiovascular events and death. Transpl Int. 2008;21(10):985-991.
    CrossRef - PubMed
  8. Dönmez A, Kayhan Z, Pirat A, Sekerci S. Anesthetic management of coronary artery bypass operation in renal transplant recipients. Transplant Proc. 1998;30(3):790-792.
    CrossRef - PubMed
  9. Moon IS, Park SC, Kim SN, Koh YB. Abdominal aortic aneurysm repair in kidney transplant recipients. Transplant Proc. 2006;38(7):2022-2024.
    CrossRef - PubMed
  10. Musci M, Yankah CA, Klose H, et al. Heart valve operations in solid organ recipients: an 18-year single-center experience. Transplantation. 2007;84(5):592-597.
    CrossRef - PubMed
  11. Sear JW. Kidney dysfunction in the postoperative period. Br J Anaesth. 2005;95(1):20-32.
    CrossRef - PubMed
  12. Englberger L, Suri RM, Greason KL, et al. Deep hypothermic circulatory arrest is not a risk factor for acute kidney injury in thoracic aortic surgery. J Thorac Cardiovasc Surg. 2011;141(2):552-558.
    CrossRef - PubMed
  13. Arnaoutakis GJ, Bihorac A, Martin TD, et al. RIFLE criteria for acute kidney injury in aortic arch surgery. J Thorac Cardiovasc Surg. 2007;134(6):1554-1560; discussion 1560-1561.
    CrossRef - PubMed
  14. Gonsowski CT, Laster MJ, Eger EI 2nd, Ferrell LD, Kerschmann RL. Toxicity of compound A in rats. Effect of a 3-hour administration. Anesthesiology. 1994;80(3):556-565.
    CrossRef - PubMed
  15. Teixeira S, Costa G, Costa F, da Silva Viana J, Mota A. Sevoflurane versus isoflurane: does it matter in renal transplantation? Transplant Proc. 2007;39(8):2486-2488.
    CrossRef - PubMed
  16. Litz RJ, Hübler M, Lorenz W, Meier VK, Albrecht DM. Renal responses to desflurane and isoflurane in patients with renal insufficiency. Anesthesiology. 2002;97(5):1133-1136.
    CrossRef - PubMed
  17. Kim WH, Lee SM, Choi JW, et al. Simplified clinical risk score to predict acute kidney injury after aortic surgery. J Cardiothorac Vasc Anesth. 2013;27(6):1158-1166.
    CrossRef - PubMed


Volume : 14
Issue : 2
Pages : 227 - 229
DOI : 10.6002/ect.2014.0100


PDF VIEW [160] KB.

From the Department of Anesthesiology and Reanimation, Inonu University, Faculty of Medicine, Malatya, Turkey
Acknowledgements: The authors have no conflicts of interest to disclose, and there was no funding for this study.
Corresponding author: Mustafa Said Aydogan, MD, Associate Professor of Anesthesiology and Reanimation, Inonu University School of Medicine, Department of Anesthesiology and Reanimation, Malatya, Turkey
Phone: +90 422 341 0660 ext: 5944
Fax: +90 422 341 0728
E-mail: dr_mustafasaid@hotmail.com