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Volume: 16 Issue: 1 February 2018

FULL TEXT

CASE REPORT
Management of a Resistant Hypotension Developing After Reperfusion of a Living-Donor Kidney Transplant

We present a case of hypotension developing after reperfusion of a living-donor kidney trans­plant and performing a graft nephrectomy and successful retransplant with the same kidney 12 hours later. Preemptive kidney transplant was performed on a 51-year-old woman who had a chronic kidney disease because of hypertension. Her 55-year-old husband was the living kidney donor. The patient was stable before reperfusion. After declamping, pink color of the transplanted kidney, thrill from the renal artery, and urinary output were seen. But shortly after reperfusion, the invasive arterial blood pressure of the patient abruptly decreased from 130/70 mm Hg to 70/40 mm Hg, her pulse was approximately 80 to 110 beats/minute. The thrill disappeared from the renal artery, but blood flow continued. A graft nephrectomy was per­formed 45 minutes after reperfusion. Invasive arterial blood pressure of the patient was stabilized at approximately 110/70 mm Hg in the intensive care unit, and the patient was retransp­lanted with the same kidney. The patient was well, with a serum creatinine level of 1.4 mg/dL, 12 months after the operation. Resistant hypotension that occurs after kidney transplant may cause a loss of the graft and the patient. To prevent graft loss, and to stabilize the patient, a graft nephrectomy and retransplant of the graft under suitable circum­stances may be considered.


Key words : Resistant hypotension, Retransplant, Graft nephrectomy, Same kidney

Introduction

Hypotension and the resulting shock is the clinical expression of insufficient oxygen delivery at the cellular level because of vascular collaps.1 When hypotension and/or shock are not treated appropriately, multiorgan failure and death may be seen.2,3 We present a case of hypotension and decreased renal perfusion developing after reperfusion of a living-donor kidney transplant and performing a graft nephrectomy and successful retransplant with the same kidney 12 hours later.

Case Report

Preemptive kidney transplant was performed on a 51-year-old woman with chronic kidney disease because of hypertension (that she had for 11 y). Her 55-year-old husband was the living kidney donor. Hot ischemia period lasted 42 seconds, cold ischemia time was 38 minutes. There were no important clinical or laboratory pathologies after routine pretransplant evaluations in either the recipient or the donor. Immunologic studies (flow cytometry crossmatch, complement-dependent cytotoxicity, and donor-specific antibodies were all negative) were suitable for the transplant. The recipient and the donor human leukocyte antigen mismatch was 5. Low-dose antithymocyte globulin protocol (0.75 mg/kg at the time of the operation and 2 consecutive days, intravenous infusion during 8 hours) and tacrolimus (0.1 mg/kg/d), mycophenolate mofetil (1 g, twice-daily), and methyl­prednisolone (1000 mg preoperatively, decreasing gradually over 5 days; and after the sixth postoperative day, prednisolone 20 mg/d was continued orally) were given as induction and maintenance therapies.

She received antihypertensive medication (amlodipine 10 mg) before the operation. Propofol (1%), atracurium besylate, and remifentanil hydro­chloride were used for the induction of anesthesia. Remifentanil infusion and sevoflurane were used for the maintenance of anesthesia. Invasive arterial blood pressure was stable at 130/70 mm Hg; her pulse was 86 beats/minute, and her central venous pressure was 12 cm H2O before reperfusion. Blood gas analysis results before perfusion were as follow: Na, 142 mmol/L; K, 5 mmol/L; Ca, 0.91 mmol/L; lactate, 1.1 mmol/L; pH, 7.33; and HCO3, 19.4 mmol/L. Before perfusion, 2500 mL 0.9% NaCl was given as an intravenous infusion. After declamping, pink color of the transplanted kidney, thrill from renal artery and urinary output were observed. But just after declamping, the invasive arterial blood pressure of the patient abruptly decreased from 130/70 mm Hg to 70/40 mm Hg and her pulse was between 80 and 110 beats/minute. Inhalation anesthetics were decreased and then closed. Dopamine (starting dose 5 mcg/kg/min and increased to 20 mcg/kg/min) and noradrenaline infusions (starting dose 2 mcg/kg/min and increased to 20 mcg/kg/min) were started as positive inotropic support because of the resistant hypotension.

The thrill at the renal artery disappeared, but blood flow continued. Ischemic changes were seen in some parts of the kidney. Perioperative renal Doppler ultrasound was performed because of the visual appearance and decreased pulse. The results of the Doppler ultrasound supported decreased vascularization of the graft kidney. We performed graft nephrectomy after both radiologic and clinical appearances of decreased vascularization of the kidney. The reasons that led us to perform graft nephrectomy were as follows: (1) To protect the graft kidney from the ischemic effects of the hypotension that might persist for a long time; (2) to follow and resuscitate the patient, and to investigate the causes of the hypotension in the surgical intensive care unit instead of in the operating room; (3) to make a wedge biopsy of the kidney to rule out possible acute rejection; and (4) we planned to perform a retransplant of the graft kidney after successful resuscitation of the patient if the biopsy results were suitable.

Second, hot ischemia was 40 seconds and cold ischemia was approximately 12 hours. The kidney was perfused by histidine-tryptophan-ketoglutarate (Custodiol) solution at the back table, and a biopsy specimen was obtained. The graft kidney was kept under an icy environment after being covered with sterile organ protecting covers. The patient was transferred to the intensive care unit. Positive inotropic support (dopamine 20 mcg/kg/min and noradrenaline 20 mcg/kg/min) and colloidal fluid support was continued in the postoperative intensive care unit. The blood pressure of the patient gradually increased postoperatively. Clinical problems such as septic shock, anaphylactic shock, pulmonary emboli, pneumothorax, pericardial tamponade, myocardial infarction, postperfusion syndrome, acute pulmonary congestion, and aortic dissection were not possible explanations for the patient’s hypotension, as indicated by the intensive clinical and radiologic investigations (abdominal ultrasound, transthoracic echocardiography, lower extremity Doppler ultra­sound, and chest radiograph).

We thought that our case had vasoplegic syndrome, but we could not prove it because the intraoperative cardiac index and systemic vascular resistance were not measured. The patient's relatives, the donor, and the National Organ and Tissue Transplantation Coordination System were informed about the condition of the patient and the graft. A histopathologic examination of the biopsy specimen did not show either rejection or ischemic changes. The invasive arterial blood pressure of the patient was stabilized at approximately 110/70 mm Hg and after getting consent, the patient was retransplanted with the same kidney 12 hours after the first operation. Ketamine and atracurium besylate as a neuromuscular blocker were used for the induction of anesthesia of the retransplant. Sevoflurane infusion adjusted according to the blood pressure was continued for maintenance of anesthesia. Hypotension was not seen after retransplant. Renal artery Doppler ultrasound showed normal renal artery flow and a resistive index of 0.7 after retransplant. Urinary output was seen after 24 hours. We continued antithymocyte globulin for 5 days and stopped tacrolimus to prevent nephrotoxicity. We restarted tacrolimus at the third postoperative day after her serum creatinine level was lower than 2 mg/dL. Positive inotropic support was gradually reduced and stopped. The patient was discharged after the 10th postoperative day. At discharge, the patient was well, with a serum creatinine level of 1.4 mg/dL 12 months after the operation.

Discussion

We present a patient with an undifferentiated hypotension developing after a living-donor kidney transplant. Hypoperfusion of the graft was observed because of hypotension, and graft nephrectomy had to be performed. After successful resuscitation in the intensive care unit, the same graft was retransplanted to the patient. As far as we know, there is no such case in the literature. Clinical findings of shock of our patient were not consistent with distributive, cardiogenic, hypovolemic, and obstructive shock features. Hypotension developing just after reper­fusion might indicate postperfusion syndrome. Postperfusion syndrome was first described in a liver transplant patient in 1987. It was defined as more than a 30% decrease in blood pressure for at least 1 minute after the first 5 minutes of reperfusion plus persistent bradycardia.

More recently, postperfusion syndrome also has been reported during several other surgeries including cardiopulmonary bypass, ischemic limb reperfusion, aneurysm repair, and most recently, renal transplant with unknown frequencies.4-7 Bruhl and associates evaluated 150 kidney transplant patients and searched for patients with a 15% decrease in their blood pressure and persistent bradycardia for the first 5 minutes of reperfusion that lasted longer than 1 minute. They found 6 patients out of 150 patients fulfilled this postperfusion syndrome criteria, and 1 of these patients had graft loss.8 Our case had hypotension just after reperfusion that lasted more than 1 minute (10 h), but she did not have persistent bradycardia, so she was incompatible with the postperfusion syndrome. Vasoplegic syndrome is usually seen after cardiac surgeries and is characterized by low invasive arterial blood pressure, high cardiac index (> 2.5 L/min/m2) and low systemic vascular resistance (< 800 dyn.s.cm-5).9,10 In our case, hypotension was seen after reperfusion, and we could not measure the cardiac index or the systemic vascular resistance intra­operatively, so we could not prove or disprove a vasoplegic syndrome in our patient.

Conclusions

Resistant undifferentiated hypotension that occurs after a kidney transplant may lead to graft and patient loss. To prevent graft loss, and to stabilize the patient, a graft nephrectomy and retransplant of the graft under suitable circumstances may be con­sidered.


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Volume : 16
Issue : 1
Pages : 96 - 98
DOI : 10.6002/ect.2015.0179


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From the 1Diyarbakir Education and Research Hospital, Transplantation Center, Diyarbakir; the 2Diyarbakýr Gazi Yaþargil Education and Research Hospital, Department of Anesthesia and Intensive Care; the 3Diyarbakýr Gazi Yaþargil Education and Research Hospital, Department of Nephrology; and the 4Diyarbakýr Gazi Yaþargil Education and Research Hospital, Department of Cardiovascular Surgery, Diyarbakýr, Turkey
Acknowledgements: The authors declare that they have no sources of funding for this study, and they have no conflicts of interest to declare.
Corresponding author: Nurettin Ay, Diyarbakir Education and Research Hospital, Transplantation Center, Diyarbakir, Turkey
Phone: +90 505 661 4260
Fax: +90 412 258 0059
E-mail: nurettinay77@hotmail.com